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mouse anti isl2 (Developmental Studies Hybridoma Bank)

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Developmental Studies Hybridoma Bank mouse anti isl2
Mouse Anti Isl2, supplied by Developmental Studies Hybridoma Bank, used in various techniques. Bioz Stars score: 94/100, based on 83 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 94 stars, based on 83 article reviews

mouse anti isl2 - by Bioz Stars, 2026-04

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Figure 1. Spatiotemporal dynamics of Isl2 expression and heterogeneity of motor neurons (MNs). (a) Uniform Manifold Approximation and Projection (UMAP) visualization of scRNA-seq data based on et al.’s study, highlighting distinct MN lineages: pMN progenitors, immature MNs, MMC, P/HMC, LMCm, LMCl, PGCa, and PGCb neurons, each depicted in distinct clusters. (b) UMAP representation showing the differential expression of Isl1 and Isl2, across MN clusters. (c) Heatmap demonstrating the dynamic gene expression profiles of Isl1, Isl2, and other marker genes within MN clusters.

Journal: eLife

Article Title: Transcriptional control of motor pool formation and motor circuit connectivity by the LIM-HD protein Isl2

doi: 10.7554/elife.84596

Figure Lengend Snippet: Figure 1. Spatiotemporal dynamics of Isl2 expression and heterogeneity of motor neurons (MNs). (a) Uniform Manifold Approximation and Projection (UMAP) visualization of scRNA-seq data based on et al.’s study, highlighting distinct MN lineages: pMN progenitors, immature MNs, MMC, P/HMC, LMCm, LMCl, PGCa, and PGCb neurons, each depicted in distinct clusters. (b) UMAP representation showing the differential expression of Isl1 and Isl2, across MN clusters. (c) Heatmap demonstrating the dynamic gene expression profiles of Isl1, Isl2, and other marker genes within MN clusters.

Article Snippet: Reagent type (species) or resource Designation Source or reference Identifiers Additional information Strain, strain background (Mouse, female) C57BL/6J Damul Science Co. Genetic reagent (Mus musculus) Isl2-/- PMID:14766174 MGI:3046260 Genetic reagent (M. musculus) Isl2flox/flox This paper MGI:109156 See Materials and methods, and Figure 3—figure supplement 1a Genetic reagent (M. musculus) Tg(Mnx1- GFP)1Slp PMID:15201216 MGI:3767834 Genetic reagent (M. musculus) B6.Cg- Tg(Thy1- YFP)16Jrs/J Jackson Laboratory PMID:11086982 RRID:IMSR_JAX:003709 Genetic reagent (M. musculus) Olig2tm1(cre)Tmj PMID:18046410 MGI:3774124 Cell line (human) 293[HEK- 293] Korean Cell Line Bank KCLB# 21573 Verified using STR profiling and confirmed to be mycoplasma- free Antibody Anti- Olig2 (guinea pig polyclonal) Jessell lab (1:8000) Antibody Anti- Hb9 (rabbit polyclonal) PMID:10471502 (1:8000) Antibody Anti- Hb9 (guinea pig polyclonal) PMID:10482235 (1:2000) Antibody Anti- GFP (mouse monoclonal) Sigma Cat# G6539 (1:2000) Antibody Anti- Isl1/2 (rabbit polyclonal) PMID:7528105 PMID:8565076 (1:5000) Antibody Anti- Isl2 (mouse monoclonal) Santa Cruz Cat# sc- 390746 (1:500) Antibody Anti- Lhx3 (guinea pig polyclonal) Pfaff lab (1:4000) Antibody Anti- ChAT (goat polyclonal) Chemicon Cat# AB144P (1:100) Antibody Anti- Foxp1 (rabbit polyclonal) Abcam Cat# ab16645 (1:5000) Antibody Anti- Nkx6.1 (goat polyclonal) R&D Systems Cat# AF5857 (1:1000) Antibody Anti- Isl1 (goat polyclonal) R&D Systems Cat# AF1837 (1:1000) Antibody Anti- Isl2 (guinea pig polyclonal) PMID:14766174 Cat# AF1837 (1:8000) Antibody Anti- Lhx1 (rabbit polyclonal) Abcam Cat# ab14554 (1:500) Antibody Anti- Scip (guinea pig polyclonal) Dasen lab (1:8000) Lee et al. eLife 2023;0:e84596.

Techniques: Expressing, Quantitative Proteomics, Gene Expression, Marker

Figure 2. Disrupted motor column organization in Isl2-null mice. (a) Spatial representation of motor neuron (MN) subtypes: median motor column (MMC) (gray, Lhx3+Hb9+), lateral motor column (LMC) (red, Foxp1+), and preganglionic column (PGC) (blue, Isl1+ nNOS+) neurons from the images in b. X and y coordinates denote the medial-to-lateral and ventral-to-dorsal axes, respectively, in μm. (b) Expression of Hb9, Lhx3, Foxp1, Isl1, nNOS, and pSMAD in E13.5 mouse embryonic spinal cords. Brackets mark ectopic MNs observed in Isl2-null mice. (c) Quantification of MMC (gray), LMC (red), hypaxial motor column (HMC) (blue), and PGC (yellow) neurons across brachial (C6–C8), lumbar (L2–L4), and thoracic spinal segments. Average MN number per mouse. Box plots illustrate distribution with median (center line), first and third quartiles (box boundaries), and 10th-90th percentiles (whiskers). Data from three mice per group, analyzed using unpaired Student’s t-test; **p<0.01; n.s. indicates not significant. Refer to Supplementary file 2 and source data for detailed statistics. Scale bars, 100 μm.

Journal: eLife

Article Title: Transcriptional control of motor pool formation and motor circuit connectivity by the LIM-HD protein Isl2

doi: 10.7554/elife.84596

Figure Lengend Snippet: Figure 2. Disrupted motor column organization in Isl2-null mice. (a) Spatial representation of motor neuron (MN) subtypes: median motor column (MMC) (gray, Lhx3+Hb9+), lateral motor column (LMC) (red, Foxp1+), and preganglionic column (PGC) (blue, Isl1+ nNOS+) neurons from the images in b. X and y coordinates denote the medial-to-lateral and ventral-to-dorsal axes, respectively, in μm. (b) Expression of Hb9, Lhx3, Foxp1, Isl1, nNOS, and pSMAD in E13.5 mouse embryonic spinal cords. Brackets mark ectopic MNs observed in Isl2-null mice. (c) Quantification of MMC (gray), LMC (red), hypaxial motor column (HMC) (blue), and PGC (yellow) neurons across brachial (C6–C8), lumbar (L2–L4), and thoracic spinal segments. Average MN number per mouse. Box plots illustrate distribution with median (center line), first and third quartiles (box boundaries), and 10th-90th percentiles (whiskers). Data from three mice per group, analyzed using unpaired Student’s t-test; **p<0.01; n.s. indicates not significant. Refer to Supplementary file 2 and source data for detailed statistics. Scale bars, 100 μm.

Techniques: Expressing

Figure 4. Altered lumbar motor column position in Isl2 mutant mice. (a) Immunofluorescence images of motor neurons (MNs) labeled with Hb9, Lhx3, Foxp1, Scip, Nkx6.1, Lhx1, Isl1, and Etv4 in adjacent sections of L2 and L4 spinal cords from Het (+/-), Isl2 knockout (KO) (-/-), and Isl2 conditional KO (cKO) (Isl2 F/-; Olig2Cre) mice. (b) Average ventro-dorsal distribution of MMC (Hb9+Lhx3+) and MMC/HMC (Hb9+Foxp1-Scip+) neurons and medio-lateral distribution of LMCm (Hb9lowNkx6.1+) and LMCl (Hb9highLhx1+) neurons in heterozygote, Isl2 KO, and Isl2 cKO embryos. n=3 mice for each genotype; SD

Journal: eLife

Article Title: Transcriptional control of motor pool formation and motor circuit connectivity by the LIM-HD protein Isl2

doi: 10.7554/elife.84596

Figure Lengend Snippet: Figure 4. Altered lumbar motor column position in Isl2 mutant mice. (a) Immunofluorescence images of motor neurons (MNs) labeled with Hb9, Lhx3, Foxp1, Scip, Nkx6.1, Lhx1, Isl1, and Etv4 in adjacent sections of L2 and L4 spinal cords from Het (+/-), Isl2 knockout (KO) (-/-), and Isl2 conditional KO (cKO) (Isl2 F/-; Olig2Cre) mice. (b) Average ventro-dorsal distribution of MMC (Hb9+Lhx3+) and MMC/HMC (Hb9+Foxp1-Scip+) neurons and medio-lateral distribution of LMCm (Hb9lowNkx6.1+) and LMCl (Hb9highLhx1+) neurons in heterozygote, Isl2 KO, and Isl2 cKO embryos. n=3 mice for each genotype; SD

Techniques: Mutagenesis, Immunofluorescence, Labeling, Knock-Out

Figure 5. Loss of Etv4 expression in Isl2-null motor neurons (MNs). (a) Expression of Isl1, Scip, and Etv4 in brachial and lumbar spinal cords of Isl2 +/-, Isl2 knockout (KO), Isl2 F/−, and Isl2 F/−; Olig2Cre animals at E11.5 and E13.5. Note that Etv4 expression vanishes in lumbar, but not in brachial MNs (arrowheads). Summary diagram depicts the position of lateral motor column (LMC) motor pools innervating the cutaneous maximus (CM), latissimus dorsi (LD), and gluteus (Gl) muscles for each genotype. Scale bars, 100 μm. (b) RT-PCR results and quantification demonstrate reduced Etv4 transcript

Journal: eLife

Article Title: Transcriptional control of motor pool formation and motor circuit connectivity by the LIM-HD protein Isl2

doi: 10.7554/elife.84596

Figure Lengend Snippet: Figure 5. Loss of Etv4 expression in Isl2-null motor neurons (MNs). (a) Expression of Isl1, Scip, and Etv4 in brachial and lumbar spinal cords of Isl2 +/-, Isl2 knockout (KO), Isl2 F/−, and Isl2 F/−; Olig2Cre animals at E11.5 and E13.5. Note that Etv4 expression vanishes in lumbar, but not in brachial MNs (arrowheads). Summary diagram depicts the position of lateral motor column (LMC) motor pools innervating the cutaneous maximus (CM), latissimus dorsi (LD), and gluteus (Gl) muscles for each genotype. Scale bars, 100 μm. (b) RT-PCR results and quantification demonstrate reduced Etv4 transcript

Techniques: Expressing, Knock-Out, Muscles, Reverse Transcription Polymerase Chain Reaction

Figure 6. Transcriptome analysis of Isl2-deficient brachial and lumbar motor neurons (MNs) at E12.5. (a, b) MA plots highlighting top differentially expressed genes (DEGs) in brachial and lumbar MNs of E12.5 Isl2-null and Isl2 +/- embryos. (c) Venn diagram depicting the overlap of downregulated genes in brachial and lumbar MNs in Isl2-null embryos. (d, e) Heatmaps illustrating selected downregulated genes in the brachial and lumbar spinal cords of Isl2-deleted embryos. (f, g) Gene ontology (GO) analysis of downregulated DEGs at the brachial and lumbar levels in Isl2 knockout (KO)

Journal: eLife

Article Title: Transcriptional control of motor pool formation and motor circuit connectivity by the LIM-HD protein Isl2

doi: 10.7554/elife.84596

Figure Lengend Snippet: Figure 6. Transcriptome analysis of Isl2-deficient brachial and lumbar motor neurons (MNs) at E12.5. (a, b) MA plots highlighting top differentially expressed genes (DEGs) in brachial and lumbar MNs of E12.5 Isl2-null and Isl2 +/- embryos. (c) Venn diagram depicting the overlap of downregulated genes in brachial and lumbar MNs in Isl2-null embryos. (d, e) Heatmaps illustrating selected downregulated genes in the brachial and lumbar spinal cords of Isl2-deleted embryos. (f, g) Gene ontology (GO) analysis of downregulated DEGs at the brachial and lumbar levels in Isl2 knockout (KO)

Techniques: Knock-Out

Figure 7. Impaired proprioceptive sensory nerve connectivity in the gluteus (Gl) motor pools of Isl2 mutant mice. (a–c) Representative images of adult lumbar spinal cords immunostainined with ChAT antibody and quantification of average number of motor neurons (MNs) (b) and their medio- lateral distribution (c). (d) Representative dendritic arbors of Gl, tensor fasciae latae (Tfl), and rectus femoris (Rf) motor pools retrogradely labeled with rhodamine-dextran (Rh-Dex). Radial (R) plots show average dendritic membrane density per octant (red bars) from motor somata (six to eight adjacent

Journal: eLife

Article Title: Transcriptional control of motor pool formation and motor circuit connectivity by the LIM-HD protein Isl2

doi: 10.7554/elife.84596

Figure Lengend Snippet: Figure 7. Impaired proprioceptive sensory nerve connectivity in the gluteus (Gl) motor pools of Isl2 mutant mice. (a–c) Representative images of adult lumbar spinal cords immunostainined with ChAT antibody and quantification of average number of motor neurons (MNs) (b) and their medio- lateral distribution (c). (d) Representative dendritic arbors of Gl, tensor fasciae latae (Tfl), and rectus femoris (Rf) motor pools retrogradely labeled with rhodamine-dextran (Rh-Dex). Radial (R) plots show average dendritic membrane density per octant (red bars) from motor somata (six to eight adjacent

Techniques: Mutagenesis, Labeling, Membrane

Figure 8. Reduced terminal motor axon branching in gluteus (Gl) muscles of Isl2 mutants. (a) Visualization of motor axons and neuromuscular junctions (NMJs) in P0 and P14 Gl muscles with Hb9::GFP (green) and α-bungarotoxin (BTX, red) immunoreactivity. Higher magnification views are provided for the boxed regions. The NMJ region is delineated by white lines in P0. Arrowheads indicate atrophic NMJs on overshooting axons in P14. (b) Number of NMJs in P0 Gl muscles (919±23 NMJs for control, vs. 772±44 for Isl2 knockout [KO], p=0.0257, n=4 muscles per group, three animals). (c) Secondary

Journal: eLife

Article Title: Transcriptional control of motor pool formation and motor circuit connectivity by the LIM-HD protein Isl2

doi: 10.7554/elife.84596

Figure Lengend Snippet: Figure 8. Reduced terminal motor axon branching in gluteus (Gl) muscles of Isl2 mutants. (a) Visualization of motor axons and neuromuscular junctions (NMJs) in P0 and P14 Gl muscles with Hb9::GFP (green) and α-bungarotoxin (BTX, red) immunoreactivity. Higher magnification views are provided for the boxed regions. The NMJ region is delineated by white lines in P0. Arrowheads indicate atrophic NMJs on overshooting axons in P14. (b) Number of NMJs in P0 Gl muscles (919±23 NMJs for control, vs. 772±44 for Isl2 knockout [KO], p=0.0257, n=4 muscles per group, three animals). (c) Secondary

Techniques: Muscles, Control, Knock-Out

Figure 9. Hindlimb gait impairment in Isl2 mutants. (a) Tail suspension test images showing rigid wide-open posture of the hindlimbs in Isl2 mutant mice. (b) Footprint patterns of 3-month-old Isl2 +/- and Isl2 knockout (KO) mice. (c) Measurement of the stride width of forelimbs (1.56±0.06 cm for Isl2 +/-, vs. 1.73±0.06 cm for Isl2 KO, p=0.0782) and hindlimbs (2.70±0.05 cm for Isl2 +/-, vs. 3.63±0.09 cm for Isl2 KO, p<0.0001). n=5–8 animals per genotype; SEM is shown; unpaired Student’s t-test; see Supplementary file 2 and source data for detailed n and statistics. ****p<0.0001, n.s.=not significant. (d) Gross appearance of lower limbs and dissected hindlimb samples of adult Isl2 +/- and Isl2 KO mice. (e) Measurement of body (9.9±0.8 g for Isl2 +/-, vs. 6.9±0.8 g for Isl2 KO, p=0.0339) and muscle weight for gluteus (GI) (67.6±12.6 mg for Isl2 +/-, vs. 34.3±2.7 mg for Isl2 KO, p=0.0316, n=5–6 muscles per group) and rectus femoris muscles (51.1±8.2 mg for Isl2 +/-, vs. 27.6±3.8 mg for Isl2 KO, p=0.0384, n=5–6 muscles per group). n=5 animals for heterozygote, n=4 animals for KO; SEM is shown; unpaired Student’s t-test; see Supplementary file 2 and source data for detailed n and statistics. *p<0.05. (f) Representative electromyographic (EMG) recordings of Gl muscles during free-walking. (g) Signature of individual footsteps. (h–j) Quantification of average frequency (861±18 Hz for Isl2 +/-, vs. 619±16 Hz for Isl2 KO, p<0.0001), number of single-motor-unit potentials (80±4 peaks for Isl2 +/-, vs. 42±3 peaks for Isl2 KO, p<0.0001), and burst activity duration (0.096±0.005 s for Isl2 +/-, vs. 0.068±0.005 s for Isl2 KO, p=0.0001) in EMG recordings of Gl muscles. Three animals per group; box plots illustrate distribution with median (center line), first and third quartiles (box boundaries),

Journal: eLife

Article Title: Transcriptional control of motor pool formation and motor circuit connectivity by the LIM-HD protein Isl2

doi: 10.7554/elife.84596

Figure Lengend Snippet: Figure 9. Hindlimb gait impairment in Isl2 mutants. (a) Tail suspension test images showing rigid wide-open posture of the hindlimbs in Isl2 mutant mice. (b) Footprint patterns of 3-month-old Isl2 +/- and Isl2 knockout (KO) mice. (c) Measurement of the stride width of forelimbs (1.56±0.06 cm for Isl2 +/-, vs. 1.73±0.06 cm for Isl2 KO, p=0.0782) and hindlimbs (2.70±0.05 cm for Isl2 +/-, vs. 3.63±0.09 cm for Isl2 KO, p<0.0001). n=5–8 animals per genotype; SEM is shown; unpaired Student’s t-test; see Supplementary file 2 and source data for detailed n and statistics. ****p<0.0001, n.s.=not significant. (d) Gross appearance of lower limbs and dissected hindlimb samples of adult Isl2 +/- and Isl2 KO mice. (e) Measurement of body (9.9±0.8 g for Isl2 +/-, vs. 6.9±0.8 g for Isl2 KO, p=0.0339) and muscle weight for gluteus (GI) (67.6±12.6 mg for Isl2 +/-, vs. 34.3±2.7 mg for Isl2 KO, p=0.0316, n=5–6 muscles per group) and rectus femoris muscles (51.1±8.2 mg for Isl2 +/-, vs. 27.6±3.8 mg for Isl2 KO, p=0.0384, n=5–6 muscles per group). n=5 animals for heterozygote, n=4 animals for KO; SEM is shown; unpaired Student’s t-test; see Supplementary file 2 and source data for detailed n and statistics. *p<0.05. (f) Representative electromyographic (EMG) recordings of Gl muscles during free-walking. (g) Signature of individual footsteps. (h–j) Quantification of average frequency (861±18 Hz for Isl2 +/-, vs. 619±16 Hz for Isl2 KO, p<0.0001), number of single-motor-unit potentials (80±4 peaks for Isl2 +/-, vs. 42±3 peaks for Isl2 KO, p<0.0001), and burst activity duration (0.096±0.005 s for Isl2 +/-, vs. 0.068±0.005 s for Isl2 KO, p=0.0001) in EMG recordings of Gl muscles. Three animals per group; box plots illustrate distribution with median (center line), first and third quartiles (box boundaries),

Techniques: Suspension, Mutagenesis, Knock-Out, Muscles, Activity Assay

( a ) Expression of Isl1, Scip, and Etv4 in brachial and lumbar spinal cords of Isl2 +/- , Isl2 knockout (KO), Isl2 F/ −, and Isl2 F/ −; Olig2 Cre animals at E11.5 and E13.5. Note that Etv4 expression vanishes in lumbar, but not in brachial MNs (arrowheads). Summary diagram depicts the position of lateral motor column (LMC) motor pools innervating the cutaneous maximus (CM), latissimus dorsi (LD), and gluteus (Gl) muscles for each genotype. Scale bars, 100 μm. ( b ) RT-PCR results and quantification demonstrate reduced Etv4 transcript levels in E12.5 Isl2- null lumbar spinal cords. Relative expression of Etv4 at brachial: 1.00±0.06 for Isl2 +/+ , 0.98±0.04 for Isl2 +/- , and 0.85±0.07 for Isl2 KO; p=0.2692 for Isl2 +/+ vs. Isl2 KO, p=0.3736 for Isl2 +/- vs. Isl2 KO; n=3 animals per genotype. Relative expression of Etv4 at lumbar: 1.00±0.08 for Isl2 +/+ , 0.96±0.08 for Isl2 +/- , and 0.54±0.07 for Isl2 KO; p=0.0020 for Isl2 +/+ vs. Isl2 KO, p=0.0024 for Isl2 +/- vs. Isl2 KO; n=6–8 animals per genotype. Box plots illustrate distribution with median (center line), first and third quartiles (box boundaries), and 10th-90th percentiles (whiskers). One-way ANOVA with Tukey’s test; see and source data for detailed n and statistics. **p<0.01, n.s.=not significant. ( c ) Expression of GFP, MNR2, ISL2, ALDH1A2 , and ETV4 in HH stage 25 chick neural tubes, electroporated with siRNA against ISL2 . Quantification analysis includes the average MNR2-expressing MNs per embryo (96±17 MNs for control, vs. 95±19 for siRNA-electroporated chick, p=0.9622), average fluorescent intensity of ISL2 expression per embryo (1.00 of relative expression ratio for control, vs. 0.65±0.06 for siRNA-electroporated side, p=0.0008), and average relative expression of ALDH1A2 per embryo (1.00 for control, vs. 0.85±0.10 for siRNA-electroporated side, p=0.3340), and average relative expression of ETV4 per embryo (1.00 for control, vs. 0.13±0.01 for siRNA-electroporated side, p<0.0001). Note that the ETV4 transcript was downregulated on the electroporated side (right; n=3–4 animals per group; SEM is shown; unpaired Student’s t-test; see and source data for detailed n and statistics). ****p<0.0001, ***p<0.001, n.s.=not significant. Scale bars, 50 μm. Figure 5—source data 1. Quantification of relative expression of Etv4 in brachial and lumbar spinal cords of wild-type, Isl2 +/- and Isl2 -null embryos for . Figure 5—source data 2. Quantification of MNR2 + cells and relative expression of ISL2, ETV4 , ALDH1A2 in chick spinal cords, electroporated with siRNA against ISL2 for . Figure 5—source data 3. Unedited raw agarose gel pictures and labeled gel pictures of RT-PCR results for .

Journal: eLife

Article Title: Transcriptional control of motor pool formation and motor circuit connectivity by the LIM-HD protein Isl2

doi: 10.7554/eLife.84596

Figure Lengend Snippet: ( a ) Expression of Isl1, Scip, and Etv4 in brachial and lumbar spinal cords of Isl2 +/- , Isl2 knockout (KO), Isl2 F/ −, and Isl2 F/ −; Olig2 Cre animals at E11.5 and E13.5. Note that Etv4 expression vanishes in lumbar, but not in brachial MNs (arrowheads). Summary diagram depicts the position of lateral motor column (LMC) motor pools innervating the cutaneous maximus (CM), latissimus dorsi (LD), and gluteus (Gl) muscles for each genotype. Scale bars, 100 μm. ( b ) RT-PCR results and quantification demonstrate reduced Etv4 transcript levels in E12.5 Isl2- null lumbar spinal cords. Relative expression of Etv4 at brachial: 1.00±0.06 for Isl2 +/+ , 0.98±0.04 for Isl2 +/- , and 0.85±0.07 for Isl2 KO; p=0.2692 for Isl2 +/+ vs. Isl2 KO, p=0.3736 for Isl2 +/- vs. Isl2 KO; n=3 animals per genotype. Relative expression of Etv4 at lumbar: 1.00±0.08 for Isl2 +/+ , 0.96±0.08 for Isl2 +/- , and 0.54±0.07 for Isl2 KO; p=0.0020 for Isl2 +/+ vs. Isl2 KO, p=0.0024 for Isl2 +/- vs. Isl2 KO; n=6–8 animals per genotype. Box plots illustrate distribution with median (center line), first and third quartiles (box boundaries), and 10th-90th percentiles (whiskers). One-way ANOVA with Tukey’s test; see and source data for detailed n and statistics. **p<0.01, n.s.=not significant. ( c ) Expression of GFP, MNR2, ISL2, ALDH1A2 , and ETV4 in HH stage 25 chick neural tubes, electroporated with siRNA against ISL2 . Quantification analysis includes the average MNR2-expressing MNs per embryo (96±17 MNs for control, vs. 95±19 for siRNA-electroporated chick, p=0.9622), average fluorescent intensity of ISL2 expression per embryo (1.00 of relative expression ratio for control, vs. 0.65±0.06 for siRNA-electroporated side, p=0.0008), and average relative expression of ALDH1A2 per embryo (1.00 for control, vs. 0.85±0.10 for siRNA-electroporated side, p=0.3340), and average relative expression of ETV4 per embryo (1.00 for control, vs. 0.13±0.01 for siRNA-electroporated side, p<0.0001). Note that the ETV4 transcript was downregulated on the electroporated side (right; n=3–4 animals per group; SEM is shown; unpaired Student’s t-test; see and source data for detailed n and statistics). ****p<0.0001, ***p<0.001, n.s.=not significant. Scale bars, 50 μm. Figure 5—source data 1. Quantification of relative expression of Etv4 in brachial and lumbar spinal cords of wild-type, Isl2 +/- and Isl2 -null embryos for . Figure 5—source data 2. Quantification of MNR2 + cells and relative expression of ISL2, ETV4 , ALDH1A2 in chick spinal cords, electroporated with siRNA against ISL2 for . Figure 5—source data 3. Unedited raw agarose gel pictures and labeled gel pictures of RT-PCR results for .

Article Snippet: The following antibodies were used: guinea pig anti-Olig2 , rabbit and guinea pig anti-HB9 , rabbit anti-GFP (Invitrogen), mouse anti-GFP (Sigma), rabbit anti-Isl1/2 , mouse anti-Isl2 (Santa Cruz), guinea pig anti-Lhx3 , goat anti-ChAT (Chemicon), rabbit anti-Foxp1 (Abcam), goat anti-Nkx6.1 (R&D Systems), goat anti-Isl1 (R&D Systems), guinea pig anti-Isl2 , rabbit anti-Lhx1 (Abcam), guinea pig anti-Scip , rabbit anti-Etv4 , rabbit anti-Tetramethylrhodamine (Invitrogen), guinea pig anti-vGluT1 (Millipore), rabbit anti-nNOS (Diasorin), and rabbit anti-pSMAD (Cell Signaling Technology).

Techniques: Expressing, Knock-Out, Muscles, Reverse Transcription Polymerase Chain Reaction, Agarose Gel Electrophoresis, Labeling

( a ) Uniform Manifold Approximation and Projection (UMAP) visualization of scRNA-seq data based on et al.’s study, highlighting distinct MN lineages: pMN progenitors, immature MNs, MMC, P/HMC, LMCm, LMCl, PGCa, and PGCb neurons, each depicted in distinct clusters. ( b ) UMAP representation showing the differential expression of Isl1 and Isl2 , across MN clusters. ( c ) Heatmap demonstrating the dynamic gene expression profiles of Isl1 , Isl2 , and other marker genes within MN clusters. ( d ) Expression of Olig2, Isl1, Isl2 , Hb9, and Lhx3 in E10.5 spinal cords. Contour plots and medio-lateral density plots highlighting Olig2 + MN progenitors (green), Olig2 + Isl1 + newborn MNs (blue), Isl2 + MNs (pink) across all spinal cord levels. Scale bars, 50 μm. ( e ) Expression of Isl1, Isl2, Lhx3, Foxp1, nNOS, Etv4, and Hb9::GFP in E12.5 spinal cords. Scale bars, 100 μm.

Journal: eLife

Article Title: Transcriptional control of motor pool formation and motor circuit connectivity by the LIM-HD protein Isl2

doi: 10.7554/eLife.84596

Figure Lengend Snippet: ( a ) Uniform Manifold Approximation and Projection (UMAP) visualization of scRNA-seq data based on et al.’s study, highlighting distinct MN lineages: pMN progenitors, immature MNs, MMC, P/HMC, LMCm, LMCl, PGCa, and PGCb neurons, each depicted in distinct clusters. ( b ) UMAP representation showing the differential expression of Isl1 and Isl2 , across MN clusters. ( c ) Heatmap demonstrating the dynamic gene expression profiles of Isl1 , Isl2 , and other marker genes within MN clusters. ( d ) Expression of Olig2, Isl1, Isl2 , Hb9, and Lhx3 in E10.5 spinal cords. Contour plots and medio-lateral density plots highlighting Olig2 + MN progenitors (green), Olig2 + Isl1 + newborn MNs (blue), Isl2 + MNs (pink) across all spinal cord levels. Scale bars, 50 μm. ( e ) Expression of Isl1, Isl2, Lhx3, Foxp1, nNOS, Etv4, and Hb9::GFP in E12.5 spinal cords. Scale bars, 100 μm.

Techniques: Expressing, Marker

( a ) Spatial representation of motor neuron (MN) subtypes: median motor column (MMC) (gray, Lhx3 + Hb9 + ), lateral motor column (LMC) (red, Foxp1 + ), and preganglionic column (PGC) (blue, Isl1 + nNOS + ) neurons from the images in b. X and y coordinates denote the medial-to-lateral and ventral-to-dorsal axes, respectively, in μm. ( b ) Expression of Hb9, Lhx3, Foxp1, Isl1, nNOS, and pSMAD in E13.5 mouse embryonic spinal cords. Brackets mark ectopic MNs observed in Isl2- null mice. ( c ) Quantification of MMC (gray), LMC (red), hypaxial motor column (HMC) (blue), and PGC (yellow) neurons across brachial (C6–C8), lumbar (L2–L4), and thoracic spinal segments. Average MN number per mouse. Box plots illustrate distribution with median (center line), first and third quartiles (box boundaries), and 10th-90th percentiles (whiskers). Data from three mice per group, analyzed using unpaired Student’s t-test; **p<0.01; n.s. indicates not significant. Refer to and source data for detailed statistics. Scale bars, 100 μm. Figure 2—source data 1. Quantification of motor neuron (MN) subtypes at E13.5 in Isl2 +/- and Isl2 -null mice, categorized by brachial, lumbar, and thoracic levels.

Journal: eLife

Article Title: Transcriptional control of motor pool formation and motor circuit connectivity by the LIM-HD protein Isl2

doi: 10.7554/eLife.84596

Figure Lengend Snippet: ( a ) Spatial representation of motor neuron (MN) subtypes: median motor column (MMC) (gray, Lhx3 + Hb9 + ), lateral motor column (LMC) (red, Foxp1 + ), and preganglionic column (PGC) (blue, Isl1 + nNOS + ) neurons from the images in b. X and y coordinates denote the medial-to-lateral and ventral-to-dorsal axes, respectively, in μm. ( b ) Expression of Hb9, Lhx3, Foxp1, Isl1, nNOS, and pSMAD in E13.5 mouse embryonic spinal cords. Brackets mark ectopic MNs observed in Isl2- null mice. ( c ) Quantification of MMC (gray), LMC (red), hypaxial motor column (HMC) (blue), and PGC (yellow) neurons across brachial (C6–C8), lumbar (L2–L4), and thoracic spinal segments. Average MN number per mouse. Box plots illustrate distribution with median (center line), first and third quartiles (box boundaries), and 10th-90th percentiles (whiskers). Data from three mice per group, analyzed using unpaired Student’s t-test; **p<0.01; n.s. indicates not significant. Refer to and source data for detailed statistics. Scale bars, 100 μm. Figure 2—source data 1. Quantification of motor neuron (MN) subtypes at E13.5 in Isl2 +/- and Isl2 -null mice, categorized by brachial, lumbar, and thoracic levels.

Techniques: Expressing

( a ) Immunofluorescence images of motor neurons (MNs) labeled with Hb9, Lhx3, Foxp1, Scip, Isl1, Lhx1, and Etv4 in adjacent sections of C6 and C8 spinal cords from Het (+/-), Isl2 knockout (KO) (-/-), and Isl2 conditional knockout (cKO) ( Isl2 F/-; Olig2 Cre ) mice. ( b ) Average ventro-dorsal distribution of MMC (Hb9 + Lhx3 + ) and MMC/HMC (Hb9 + Foxp1 - Scip + ) neurons, and medio-lateral distribution of LMCm (Hb9 low Isl1 + ) and LMCl (Hb9 high Lhx1 + ) neurons in embryos with each genotype. n=3 mice for each genotype; standard deviation (SD) is shown; one-way ANOVA with Bonferroni’s post hoc test; Het vs. KO or cKO, **p<0.01, *p<0.05. ( c ) Average cell count per embryo in flexor carpi ulnaris (FCU) (Foxp1 + Scip + ), cutaneous maximus (CM) (Isl1 + Etv4 + ), and latissimus dorsi (LD) (Isl1 − Etv4 + ) motor pools. Box plots illustrate distribution with median (center line), first and third quartiles (box boundaries), and 10th-90th percentiles (whiskers). One-way ANOVA with Bonferroni’s post hoc test; n.s. indicates not significant. See and source data for detailed n and statistics. Scale bar, 100 μm. Figure 3—source data 1. Average ventro-dorsal distribution of MMC (Hb9 + Lhx3 + ) and MMC/HMC (Hb9 + Foxp1 - Scip + ) neurons as well as medio-lateral distribution of LMCm (Hb9 low Isl1 + ) and LMCl (Hb9 high Lhx1 + ) neurons . It also includes the average cell count per embryo in flexor carpi ulnaris (FCU) (Foxp1 + Scip + ), cutaneous maximus (CM) (Isl1 + Etv4 + ), and latissimus dorsi (LD) (Isl1 - Etv4 + ) motor pools .

Journal: eLife

Article Title: Transcriptional control of motor pool formation and motor circuit connectivity by the LIM-HD protein Isl2

doi: 10.7554/eLife.84596

Figure Lengend Snippet: ( a ) Immunofluorescence images of motor neurons (MNs) labeled with Hb9, Lhx3, Foxp1, Scip, Isl1, Lhx1, and Etv4 in adjacent sections of C6 and C8 spinal cords from Het (+/-), Isl2 knockout (KO) (-/-), and Isl2 conditional knockout (cKO) ( Isl2 F/-; Olig2 Cre ) mice. ( b ) Average ventro-dorsal distribution of MMC (Hb9 + Lhx3 + ) and MMC/HMC (Hb9 + Foxp1 - Scip + ) neurons, and medio-lateral distribution of LMCm (Hb9 low Isl1 + ) and LMCl (Hb9 high Lhx1 + ) neurons in embryos with each genotype. n=3 mice for each genotype; standard deviation (SD) is shown; one-way ANOVA with Bonferroni’s post hoc test; Het vs. KO or cKO, **p<0.01, *p<0.05. ( c ) Average cell count per embryo in flexor carpi ulnaris (FCU) (Foxp1 + Scip + ), cutaneous maximus (CM) (Isl1 + Etv4 + ), and latissimus dorsi (LD) (Isl1 − Etv4 + ) motor pools. Box plots illustrate distribution with median (center line), first and third quartiles (box boundaries), and 10th-90th percentiles (whiskers). One-way ANOVA with Bonferroni’s post hoc test; n.s. indicates not significant. See and source data for detailed n and statistics. Scale bar, 100 μm. Figure 3—source data 1. Average ventro-dorsal distribution of MMC (Hb9 + Lhx3 + ) and MMC/HMC (Hb9 + Foxp1 - Scip + ) neurons as well as medio-lateral distribution of LMCm (Hb9 low Isl1 + ) and LMCl (Hb9 high Lhx1 + ) neurons . It also includes the average cell count per embryo in flexor carpi ulnaris (FCU) (Foxp1 + Scip + ), cutaneous maximus (CM) (Isl1 + Etv4 + ), and latissimus dorsi (LD) (Isl1 - Etv4 + ) motor pools .

Techniques: Immunofluorescence, Labeling, Knock-Out, Standard Deviation, Cell Counting

( a ) Contour or medio-lateral density plots illustrate the distribution of Hb9 + somatic MNs (sMNs, green), Hb9 + Lhx3 + MMC neurons (gray), Hb9 + Foxp1 - Scip + MMC/HMC neurons (yellow), Hb9 + Foxp1 + LMC neurons (purple); Hb9 low Isl1 + LMCm neurons (skyblue), Hb9 high Lhx1 + LMCl neurons (magenta), Foxp1 + Scip + flexor carpi ulnaris (FCU) (orange), Isl1 + Etv4 + cutaneous maximus (CM) (blue), and Isl1 − Etv4 + latissimus dorsi (LD) (red) within C6 and C8 spinal cords of heterozygote, Isl2 knockout (KO), and Isl2 conditional knockout (cKO) mice. X and y coordinates on medial-to-lateral and ventral-to-dorsal axes in contour plots are shown in μm.

Journal: eLife

Article Title: Transcriptional control of motor pool formation and motor circuit connectivity by the LIM-HD protein Isl2

doi: 10.7554/eLife.84596

Figure Lengend Snippet: ( a ) Contour or medio-lateral density plots illustrate the distribution of Hb9 + somatic MNs (sMNs, green), Hb9 + Lhx3 + MMC neurons (gray), Hb9 + Foxp1 - Scip + MMC/HMC neurons (yellow), Hb9 + Foxp1 + LMC neurons (purple); Hb9 low Isl1 + LMCm neurons (skyblue), Hb9 high Lhx1 + LMCl neurons (magenta), Foxp1 + Scip + flexor carpi ulnaris (FCU) (orange), Isl1 + Etv4 + cutaneous maximus (CM) (blue), and Isl1 − Etv4 + latissimus dorsi (LD) (red) within C6 and C8 spinal cords of heterozygote, Isl2 knockout (KO), and Isl2 conditional knockout (cKO) mice. X and y coordinates on medial-to-lateral and ventral-to-dorsal axes in contour plots are shown in μm.

Techniques: Knock-Out

( a ) Scatter or medio-lateral density plots illustrate the distribution of Hb9 + somatic motor neurons (MNs) (sMNs, green), Hb9 + Lhx3 + MMC neurons (gray), Hb9 + Foxp1 - Scip + MMC/HMC neurons (yellow), Hb9 + Foxp1 + LMC neurons (purple); Hb9 low Isl1 + LMCm neurons (skyblue), Hb9 high Lhx1 + LMCl neurons (magenta), Foxp1 + Scip + flexor carpi ulnaris (FCU) (orange), Isl1 + Etv4 + cutaneous maximus (CM) (blue), and Isl1 − Etv4 + latissimus dorsi (LD) (red) within C6 and C8 spinal cords of heterozygote, Isl2 knockout (KO), and Isl2 cKO mice. X and y coordinates on medial-to-lateral and ventral-to-dorsal axes in scatter plots are shown in μm.

Journal: eLife

Article Title: Transcriptional control of motor pool formation and motor circuit connectivity by the LIM-HD protein Isl2

doi: 10.7554/eLife.84596

Figure Lengend Snippet: ( a ) Scatter or medio-lateral density plots illustrate the distribution of Hb9 + somatic motor neurons (MNs) (sMNs, green), Hb9 + Lhx3 + MMC neurons (gray), Hb9 + Foxp1 - Scip + MMC/HMC neurons (yellow), Hb9 + Foxp1 + LMC neurons (purple); Hb9 low Isl1 + LMCm neurons (skyblue), Hb9 high Lhx1 + LMCl neurons (magenta), Foxp1 + Scip + flexor carpi ulnaris (FCU) (orange), Isl1 + Etv4 + cutaneous maximus (CM) (blue), and Isl1 − Etv4 + latissimus dorsi (LD) (red) within C6 and C8 spinal cords of heterozygote, Isl2 knockout (KO), and Isl2 cKO mice. X and y coordinates on medial-to-lateral and ventral-to-dorsal axes in scatter plots are shown in μm.

Techniques: Knock-Out

( a ) Immunofluorescence images of motor neurons (MNs) labeled with Hb9, Lhx3, Foxp1, Scip, Nkx6.1, Lhx1, Isl1, and Etv4 in adjacent sections of L2 and L4 spinal cords from Het (+/-), Isl2 knockout (KO) (-/-), and Isl2 conditional KO (cKO) ( Isl2 F/-; Olig2 Cre ) mice. ( b ) Average ventro-dorsal distribution of MMC (Hb9 + Lhx3 + ) and MMC/HMC (Hb9 + Foxp1 - Scip + ) neurons and medio-lateral distribution of LMCm (Hb9 low Nkx6.1 + ) and LMCl (Hb9 high Lhx1 + ) neurons in heterozygote, Isl2 KO, and Isl2 cKO embryos. n=3 mice for each genotype; SD is shown; one-way ANOVA with Bonferroni’s post hoc test; **p<0.01, *p<0.05. See and source data for detailed n and statistics. ( c ) The average cell count per embryo in Etv4 + rectus femoris (Rf)/tensor fasciae latae (Tfl)/gluteus (Gl) and Nkx6.1 + Lhx1 + Ta motor pools. n=3 mice for each genotype; SEM is shown; one-way ANOVA with Bonferroni’s post hoc test, ***p<0.001, n.s.=not significant. Box plots illustrate data distribution with median (center line), first and third quartiles (box boundaries), and 10th-90th percentiles (whiskers). See and source data for detailed n and statistics. ( d ) Summary diagram depicting the position of major lumbar motor pools: rectus femoris ( R ), tensor fascia latae ( T ), tibialis anterior (Ta), and Gl. Misspecified motor pools are marked with asterisks. Scale bar, 100 μm. Figure 4—source data 1. Average ventro-dorsal distribution of MMC (Hb9 + Lhx3 + ) and MMC/HMC (Hb9 + Foxp1 - Scip + ) neurons, as well as the medio-lateral distribution of LMCm (Hb9 low Nkx6.1 + ) and LMCl (Hb9 high Lhx1 + ) neurons . It also includes the average cell count per embryo in Etv4 + rectus femoris (Rf)/tensor fasciae latae (Tfl)/gluteus (Gl) and Nkx6.1 + Lhx1 + tibialis anterior (Ta) motor pools .

Journal: eLife

Article Title: Transcriptional control of motor pool formation and motor circuit connectivity by the LIM-HD protein Isl2

doi: 10.7554/eLife.84596

Figure Lengend Snippet: ( a ) Immunofluorescence images of motor neurons (MNs) labeled with Hb9, Lhx3, Foxp1, Scip, Nkx6.1, Lhx1, Isl1, and Etv4 in adjacent sections of L2 and L4 spinal cords from Het (+/-), Isl2 knockout (KO) (-/-), and Isl2 conditional KO (cKO) ( Isl2 F/-; Olig2 Cre ) mice. ( b ) Average ventro-dorsal distribution of MMC (Hb9 + Lhx3 + ) and MMC/HMC (Hb9 + Foxp1 - Scip + ) neurons and medio-lateral distribution of LMCm (Hb9 low Nkx6.1 + ) and LMCl (Hb9 high Lhx1 + ) neurons in heterozygote, Isl2 KO, and Isl2 cKO embryos. n=3 mice for each genotype; SD is shown; one-way ANOVA with Bonferroni’s post hoc test; **p<0.01, *p<0.05. See and source data for detailed n and statistics. ( c ) The average cell count per embryo in Etv4 + rectus femoris (Rf)/tensor fasciae latae (Tfl)/gluteus (Gl) and Nkx6.1 + Lhx1 + Ta motor pools. n=3 mice for each genotype; SEM is shown; one-way ANOVA with Bonferroni’s post hoc test, ***p<0.001, n.s.=not significant. Box plots illustrate data distribution with median (center line), first and third quartiles (box boundaries), and 10th-90th percentiles (whiskers). See and source data for detailed n and statistics. ( d ) Summary diagram depicting the position of major lumbar motor pools: rectus femoris ( R ), tensor fascia latae ( T ), tibialis anterior (Ta), and Gl. Misspecified motor pools are marked with asterisks. Scale bar, 100 μm. Figure 4—source data 1. Average ventro-dorsal distribution of MMC (Hb9 + Lhx3 + ) and MMC/HMC (Hb9 + Foxp1 - Scip + ) neurons, as well as the medio-lateral distribution of LMCm (Hb9 low Nkx6.1 + ) and LMCl (Hb9 high Lhx1 + ) neurons . It also includes the average cell count per embryo in Etv4 + rectus femoris (Rf)/tensor fasciae latae (Tfl)/gluteus (Gl) and Nkx6.1 + Lhx1 + tibialis anterior (Ta) motor pools .

Techniques: Immunofluorescence, Labeling, Knock-Out, Cell Counting

( a ) Contour plots and medio-lateral density plots display the spatial distribution of Hb9 + somatic MNs (sMNs, green), Hb9 + Lhx3 + MMC neurons (gray), Hb9 + Foxp1 - Scip + MMC/HMC neurons (yellow), Hb9 + Foxp1 + LMC neurons (purple); Hb9 low Nkx6.1 + LMCm neurons (skyblue), Hb9 high Lhx1 + LMCl neurons (magenta), Hb9 + Isl1 - Etv4 + rectus femoris (Rf)/tensor fasciae latae (Tfl) and gluteus (Gl) (red), and Hb9 + Nkx6.1 + Lhx1 + Ta (blue) across L2 and L4 spinal cords in heterozygote, Isl2 knockout (KO), and Isl2 conditional KO (cKO) mice. X and y coordinates on medial-to-lateral and ventral-to-dorsal axes in contour plots are shown in μm.

Journal: eLife

Article Title: Transcriptional control of motor pool formation and motor circuit connectivity by the LIM-HD protein Isl2

doi: 10.7554/eLife.84596

Figure Lengend Snippet: ( a ) Contour plots and medio-lateral density plots display the spatial distribution of Hb9 + somatic MNs (sMNs, green), Hb9 + Lhx3 + MMC neurons (gray), Hb9 + Foxp1 - Scip + MMC/HMC neurons (yellow), Hb9 + Foxp1 + LMC neurons (purple); Hb9 low Nkx6.1 + LMCm neurons (skyblue), Hb9 high Lhx1 + LMCl neurons (magenta), Hb9 + Isl1 - Etv4 + rectus femoris (Rf)/tensor fasciae latae (Tfl) and gluteus (Gl) (red), and Hb9 + Nkx6.1 + Lhx1 + Ta (blue) across L2 and L4 spinal cords in heterozygote, Isl2 knockout (KO), and Isl2 conditional KO (cKO) mice. X and y coordinates on medial-to-lateral and ventral-to-dorsal axes in contour plots are shown in μm.

Techniques: Knock-Out

( a ) Scatter plots and medio-lateral density plots display the spatial distribution of Hb9 + somatic motor neurons (MNs) (sMNs, green), Hb9 + Lhx3 + MMC neurons (gray), Hb9 + Foxp1 - Scip + MMC/HMC neurons (yellow), Hb9 + Foxp1 + LMC neurons (purple); Hb9 low Nkx6.1 + LMCm neurons (skyblue), Hb9 high Lhx1 + LMCl neurons (magenta), Hb9 + Isl1 - Etv4 + rectus femoris (Rf)/tensor fasciae latae (Tfl) and gluteus (Gl) (red), and Hb9 + Nkx6.1 + Lhx1 + Ta (blue) across L2 and L4 spinal cords in heterozygote, Isl2 knockout (KO), and Isl2 conditional KO (cKO) mice. X and y coordinates on medial-to-lateral and ventral-to-dorsal axes in scatter plots are shown in μm.

Journal: eLife

Article Title: Transcriptional control of motor pool formation and motor circuit connectivity by the LIM-HD protein Isl2

doi: 10.7554/eLife.84596

Figure Lengend Snippet: ( a ) Scatter plots and medio-lateral density plots display the spatial distribution of Hb9 + somatic motor neurons (MNs) (sMNs, green), Hb9 + Lhx3 + MMC neurons (gray), Hb9 + Foxp1 - Scip + MMC/HMC neurons (yellow), Hb9 + Foxp1 + LMC neurons (purple); Hb9 low Nkx6.1 + LMCm neurons (skyblue), Hb9 high Lhx1 + LMCl neurons (magenta), Hb9 + Isl1 - Etv4 + rectus femoris (Rf)/tensor fasciae latae (Tfl) and gluteus (Gl) (red), and Hb9 + Nkx6.1 + Lhx1 + Ta (blue) across L2 and L4 spinal cords in heterozygote, Isl2 knockout (KO), and Isl2 conditional KO (cKO) mice. X and y coordinates on medial-to-lateral and ventral-to-dorsal axes in scatter plots are shown in μm.

Techniques: Knock-Out

Original unprocessed RT-PCR images for Gapdh and Etv4 in brachial and lumbar spinal cords of E12.5 wild-type, Isl2 +/- , and Isl2 -null embryos.

Journal: eLife

Article Title: Transcriptional control of motor pool formation and motor circuit connectivity by the LIM-HD protein Isl2

doi: 10.7554/eLife.84596

Figure Lengend Snippet: Original unprocessed RT-PCR images for Gapdh and Etv4 in brachial and lumbar spinal cords of E12.5 wild-type, Isl2 +/- , and Isl2 -null embryos.

Techniques: Reverse Transcription Polymerase Chain Reaction

( a, b ) MA plots highlighting top differentially expressed genes (DEGs) in brachial and lumbar MNs of E12.5 Isl2 -null and Isl2 +/- embryos. ( c ) Venn diagram depicting the overlap of downregulated genes in brachial and lumbar MNs in Isl2 -null embryos. ( d, e ) Heatmaps illustrating selected downregulated genes in the brachial and lumbar spinal cords of Isl2 -deleted embryos. ( f, g ) Gene ontology (GO) analysis of downregulated DEGs at the brachial and lumbar levels in Isl2 knockout (KO) embryos. ( h ) In situ hybridization and immunohistochemistry of selected downregulated genes in E12.5 Isl2 -deficient lumbar spinal cords. Dotted lines indicate the position of LMCm and LMCl. Data points of the graphs indicate normalized read counts from individual animals. SEM is shown. ( i ) Expression assessment of Epha3, Fgf10, and Sema5a, genes enriched in sb.LMCl.2 subcluster from scRNA-seq analysis in . Scale bars, 50 μm.

Journal: eLife

Article Title: Transcriptional control of motor pool formation and motor circuit connectivity by the LIM-HD protein Isl2

doi: 10.7554/eLife.84596

Figure Lengend Snippet: ( a, b ) MA plots highlighting top differentially expressed genes (DEGs) in brachial and lumbar MNs of E12.5 Isl2 -null and Isl2 +/- embryos. ( c ) Venn diagram depicting the overlap of downregulated genes in brachial and lumbar MNs in Isl2 -null embryos. ( d, e ) Heatmaps illustrating selected downregulated genes in the brachial and lumbar spinal cords of Isl2 -deleted embryos. ( f, g ) Gene ontology (GO) analysis of downregulated DEGs at the brachial and lumbar levels in Isl2 knockout (KO) embryos. ( h ) In situ hybridization and immunohistochemistry of selected downregulated genes in E12.5 Isl2 -deficient lumbar spinal cords. Dotted lines indicate the position of LMCm and LMCl. Data points of the graphs indicate normalized read counts from individual animals. SEM is shown. ( i ) Expression assessment of Epha3, Fgf10, and Sema5a, genes enriched in sb.LMCl.2 subcluster from scRNA-seq analysis in . Scale bars, 50 μm.

Techniques: Knock-Out, In Situ Hybridization, Immunohistochemistry, Expressing

( a ) scRNA-seq data based on Amin et al.’s study. Violin plots illustrating motor neuron (MN) subtype markers ( Chat , Isl1 , Isl2 , Mnx1 , Foxp1 , Lhx1 , Nkx6-1 , and Nkx6-2 ) in LMCm and LMCl clusters. ND, not defined. ( b ) Uniform Manifold Approximation and Projection (UMAP) plot displaying lumbar LMC cluster cells. ( c ) Heatmap showing marker genes for MN subtypes and motor pools of six clusters. ( d ) UMAP plots showing gene expression of LMC and motor pool markers. ( e ) Heatmap showing marker genes for sb.LMCl.1.ta and sb.LMCl.1.v. ( f ) Dot plot showing expression patterns of MN markers of LMC subclusters. ( g ) Violin plots depicting Hox genes expression in LMC subclusters. ( h ) Summary of markers of LMC subclusters. ( i ) Violin plots illustrating selected differentially expressed genes (DEGs) downregulated in Isl2 -deficient spinal cords.

Journal: eLife

Article Title: Transcriptional control of motor pool formation and motor circuit connectivity by the LIM-HD protein Isl2

doi: 10.7554/eLife.84596

Figure Lengend Snippet: ( a ) scRNA-seq data based on Amin et al.’s study. Violin plots illustrating motor neuron (MN) subtype markers ( Chat , Isl1 , Isl2 , Mnx1 , Foxp1 , Lhx1 , Nkx6-1 , and Nkx6-2 ) in LMCm and LMCl clusters. ND, not defined. ( b ) Uniform Manifold Approximation and Projection (UMAP) plot displaying lumbar LMC cluster cells. ( c ) Heatmap showing marker genes for MN subtypes and motor pools of six clusters. ( d ) UMAP plots showing gene expression of LMC and motor pool markers. ( e ) Heatmap showing marker genes for sb.LMCl.1.ta and sb.LMCl.1.v. ( f ) Dot plot showing expression patterns of MN markers of LMC subclusters. ( g ) Violin plots depicting Hox genes expression in LMC subclusters. ( h ) Summary of markers of LMC subclusters. ( i ) Violin plots illustrating selected differentially expressed genes (DEGs) downregulated in Isl2 -deficient spinal cords.

Techniques: Marker, Expressing

( a ) Whole-mount immunostaining of GFP antibody in forelimbs and hindlimbs of E12.5 and E13.5 Isl2 +/- and Isl2 knockout (KO) embryos. ( b ) Diagram of nerve trunks in the hindlimb. Hb9-driven GFP-labeled axons show major nerve trunks leading to target muscles. The femoral ( F ) nerve trunk gives rise to branches targeting the rectus femoris (Rf) and vasti ( V ) muscles, while the peroneal ( P ) nerve trunk produces branches targeting the gluteus (Gl) and tibialis anterior (Ta) muscles. ( c ) E13.0 Isl2 +/- and Isl2 KO embryos showing spinal motor nerve projection labeled with Hb9::GFP. dPN, deep peroneal; F, femoral; Gl, gluteus; Obt, obturator; PN, peroneal nerve; rad, radial; Rf, rectus femoris; Sp, superficial peroneal; T, tibialis; Ta, tibialis anterior; TN, tibial nerve; V, vasti. ( d ) Expression of Ret and Gfrα1 in Isl2 +/- and Isl2 KO embryos. Scale bars as indicated and 100 μm in ( d ).

Journal: eLife

Article Title: Transcriptional control of motor pool formation and motor circuit connectivity by the LIM-HD protein Isl2

doi: 10.7554/eLife.84596

Figure Lengend Snippet: ( a ) Whole-mount immunostaining of GFP antibody in forelimbs and hindlimbs of E12.5 and E13.5 Isl2 +/- and Isl2 knockout (KO) embryos. ( b ) Diagram of nerve trunks in the hindlimb. Hb9-driven GFP-labeled axons show major nerve trunks leading to target muscles. The femoral ( F ) nerve trunk gives rise to branches targeting the rectus femoris (Rf) and vasti ( V ) muscles, while the peroneal ( P ) nerve trunk produces branches targeting the gluteus (Gl) and tibialis anterior (Ta) muscles. ( c ) E13.0 Isl2 +/- and Isl2 KO embryos showing spinal motor nerve projection labeled with Hb9::GFP. dPN, deep peroneal; F, femoral; Gl, gluteus; Obt, obturator; PN, peroneal nerve; rad, radial; Rf, rectus femoris; Sp, superficial peroneal; T, tibialis; Ta, tibialis anterior; TN, tibial nerve; V, vasti. ( d ) Expression of Ret and Gfrα1 in Isl2 +/- and Isl2 KO embryos. Scale bars as indicated and 100 μm in ( d ).

Techniques: Immunostaining, Knock-Out, Labeling, Muscles, Expressing

( a ) Visualization of motor axons and NMJs in E18.5 Gl muscles with Thy1::YFP (green) and α-bungarotoxin (BTX, red) immunoreactivity. Scale bar, 200 μm. ( b ) Higher magnification views of various NMJs showing abnormal features, such as elongated NMJs (arrowheads) or NMJs in contact with primary axon shaft (arrow), in Isl2 cKO. Scale bar, 20 μm.

Journal: eLife

Article Title: Transcriptional control of motor pool formation and motor circuit connectivity by the LIM-HD protein Isl2

doi: 10.7554/eLife.84596

Figure Lengend Snippet: ( a ) Visualization of motor axons and NMJs in E18.5 Gl muscles with Thy1::YFP (green) and α-bungarotoxin (BTX, red) immunoreactivity. Scale bar, 200 μm. ( b ) Higher magnification views of various NMJs showing abnormal features, such as elongated NMJs (arrowheads) or NMJs in contact with primary axon shaft (arrow), in Isl2 cKO. Scale bar, 20 μm.

Techniques: Muscles

( a ) Visualization of motor axons and neuromuscular junctions (NMJs) in P0 and P14 Gl muscles with Hb9::GFP (green) and α-bungarotoxin (BTX, red) immunoreactivity. Higher magnification views are provided for the boxed regions. The NMJ region is delineated by white lines in P0. Arrowheads indicate atrophic NMJs on overshooting axons in P14. ( b ) Number of NMJs in P0 Gl muscles (919±23 NMJs for control, vs. 772±44 for Isl2 knockout [KO], p=0.0257, n=4 muscles per group, three animals). ( c ) Secondary branch length (313±17 μm for control, vs. 92±8 μm for Isl2 KO, p<0.0001, n=90–120 axons per group, three animals) in P0 Gl muscles. ( d ) End plate area covered by motor axons (1.66±0.15 mm 2 for control, vs. 0.92±0.06 mm 2 for Isl2 KO, p=0.0014, n=4–5 muscles per group, three animals) in P0 Gl muscles. ( e ) End plate area covered by AChR clusters (1.04±0.05 mm 2 for control, vs. 0.61±0.05 mm 2 for Isl2 KO, p=0.0005, n=4–5 muscles per group, three animals) in P0 Gl muscles. ( f ) The number of AChR clusters (828±45 NMJs for Isl2 +/- , vs. 104±18 for Isl2 KO, p<0.0001, n=4 muscles per group, three animals) in P14 Gl muscles. ( g ) Axons extending beyond AChR clusters at P14 (0.26±0.07 axons for Isl2 +/- , vs. 3.92±0.29 for Isl2 KO, p<0.0001, n=39–46 100 μm intervals of end plate per group, three animals). ( h ) Visualization of motor axons and NMJs in P0, P14, and P28 tensor fasciae latae (Tfl) muscles. ( i ) The number of NMJs at P14 Tfl muscles (324±35 NMJs for Isl2 +/- vs. 34±5 for Isl2 KO, p=0.0002, n=4 muscles per group, three animals). ( j ) The number of axonal inputs in P28 Tfl muscles (1.09±0.09 axons for Isl2 +/- , vs. 4.08±0.40 axons for Isl2 KO, p<0.0001, n=11–13 NMJs per group, three animals). ( k ) Representative examples of NMJs with morphological defects at higher magnification in Gl muscles at P14. For compactness and fragmentation analysis, P28 NMJs were analyzed. A swelling axon is indicated by an arrowhead. (l–r) Percentage of faint NMJs (1.12 ± 0.48% for Isl2 +/- , vs. 70.47 ± 3.22% for Isl2 KO, p<0.0001, n=16–17 random fields per group), polyinnervated NMJs (0.81 ± 0.26% for Isl2 +/- , vs. 18.49 ± 2.75% for Isl2 KO, p<0.0001, n=8–17 random fields per group), number of axonal inputs (1.05±0.05 axons for Isl2 +/- , vs. 3.91±0.25 axons for Isl2 KO, p<0.0001, n=11–22 NMJs per group), area of AChR clusters (357±11 μm 2 for Isl2 +/- , vs. 701±57 μm 2 for Isl2 KO, p<0.0001, n=11–22 NMJs per group) and nerve terminal (270±10 μm 2 for Isl2 +/- , vs. 696±63 μm 2 for Isl2 KO, p<0.0001, n=11–22 NMJs per group), percentage of denervated NMJs (0.08 ± 0.08% for Isl2 +/- , vs. 4.95 ± 1.04% for Isl2 KO, p<0.0001, n=16–17 random fields per group), compactness (81.78 ± 1.07% for Isl2 +/- , vs. 55.52 ± 1.99% for Isl2 KO, p<0.0001, n=15–39 NMJs per group) and fragmentation (0.06±0.03 for Isl2 +/- , vs. 0.78±0.06 for Isl2 KO, p<0.0001, n=15–39 NMJs per group) of AChR clusters were measured. n=3 animals per group; box plots illustrate distribution with median (center line), first and third quartiles (box boundaries), and 10th and 90th percentiles (whisker); unpaired Student’s t-test in b - f , and o ; Mann-Whitney test in g , j , l - n and p - r ; see and source data for detailed n and statistics. ****p<0.0001, ***p<0.001, **p<0.01, *p<0.05, n.s.=not significant. Scale bars: ( a ) 200 μm (for low-magnification images) and 50 μm (for high-magnification images), ( h ) 20 μm in P0, 100 μm in P14, and 10 μm in P28. ( k ) 10 μm. Figure 8—source data 1. Quantification of gluteus (Gl) neuromuscular junctions (NMJs) in Isl2 +/- and Isl2 knockout (KO) mice for . Figure 8—source data 2. Quantification of tensor fasciae latae (Tfl) neuromuscular junctions (NMJs) in Isl2 +/- and Isl2 knockout (KO) mice for .

Journal: eLife

Article Title: Transcriptional control of motor pool formation and motor circuit connectivity by the LIM-HD protein Isl2

doi: 10.7554/eLife.84596

Figure Lengend Snippet: ( a ) Visualization of motor axons and neuromuscular junctions (NMJs) in P0 and P14 Gl muscles with Hb9::GFP (green) and α-bungarotoxin (BTX, red) immunoreactivity. Higher magnification views are provided for the boxed regions. The NMJ region is delineated by white lines in P0. Arrowheads indicate atrophic NMJs on overshooting axons in P14. ( b ) Number of NMJs in P0 Gl muscles (919±23 NMJs for control, vs. 772±44 for Isl2 knockout [KO], p=0.0257, n=4 muscles per group, three animals). ( c ) Secondary branch length (313±17 μm for control, vs. 92±8 μm for Isl2 KO, p<0.0001, n=90–120 axons per group, three animals) in P0 Gl muscles. ( d ) End plate area covered by motor axons (1.66±0.15 mm 2 for control, vs. 0.92±0.06 mm 2 for Isl2 KO, p=0.0014, n=4–5 muscles per group, three animals) in P0 Gl muscles. ( e ) End plate area covered by AChR clusters (1.04±0.05 mm 2 for control, vs. 0.61±0.05 mm 2 for Isl2 KO, p=0.0005, n=4–5 muscles per group, three animals) in P0 Gl muscles. ( f ) The number of AChR clusters (828±45 NMJs for Isl2 +/- , vs. 104±18 for Isl2 KO, p<0.0001, n=4 muscles per group, three animals) in P14 Gl muscles. ( g ) Axons extending beyond AChR clusters at P14 (0.26±0.07 axons for Isl2 +/- , vs. 3.92±0.29 for Isl2 KO, p<0.0001, n=39–46 100 μm intervals of end plate per group, three animals). ( h ) Visualization of motor axons and NMJs in P0, P14, and P28 tensor fasciae latae (Tfl) muscles. ( i ) The number of NMJs at P14 Tfl muscles (324±35 NMJs for Isl2 +/- vs. 34±5 for Isl2 KO, p=0.0002, n=4 muscles per group, three animals). ( j ) The number of axonal inputs in P28 Tfl muscles (1.09±0.09 axons for Isl2 +/- , vs. 4.08±0.40 axons for Isl2 KO, p<0.0001, n=11–13 NMJs per group, three animals). ( k ) Representative examples of NMJs with morphological defects at higher magnification in Gl muscles at P14. For compactness and fragmentation analysis, P28 NMJs were analyzed. A swelling axon is indicated by an arrowhead. (l–r) Percentage of faint NMJs (1.12 ± 0.48% for Isl2 +/- , vs. 70.47 ± 3.22% for Isl2 KO, p<0.0001, n=16–17 random fields per group), polyinnervated NMJs (0.81 ± 0.26% for Isl2 +/- , vs. 18.49 ± 2.75% for Isl2 KO, p<0.0001, n=8–17 random fields per group), number of axonal inputs (1.05±0.05 axons for Isl2 +/- , vs. 3.91±0.25 axons for Isl2 KO, p<0.0001, n=11–22 NMJs per group), area of AChR clusters (357±11 μm 2 for Isl2 +/- , vs. 701±57 μm 2 for Isl2 KO, p<0.0001, n=11–22 NMJs per group) and nerve terminal (270±10 μm 2 for Isl2 +/- , vs. 696±63 μm 2 for Isl2 KO, p<0.0001, n=11–22 NMJs per group), percentage of denervated NMJs (0.08 ± 0.08% for Isl2 +/- , vs. 4.95 ± 1.04% for Isl2 KO, p<0.0001, n=16–17 random fields per group), compactness (81.78 ± 1.07% for Isl2 +/- , vs. 55.52 ± 1.99% for Isl2 KO, p<0.0001, n=15–39 NMJs per group) and fragmentation (0.06±0.03 for Isl2 +/- , vs. 0.78±0.06 for Isl2 KO, p<0.0001, n=15–39 NMJs per group) of AChR clusters were measured. n=3 animals per group; box plots illustrate distribution with median (center line), first and third quartiles (box boundaries), and 10th and 90th percentiles (whisker); unpaired Student’s t-test in b - f , and o ; Mann-Whitney test in g , j , l - n and p - r ; see and source data for detailed n and statistics. ****p<0.0001, ***p<0.001, **p<0.01, *p<0.05, n.s.=not significant. Scale bars: ( a ) 200 μm (for low-magnification images) and 50 μm (for high-magnification images), ( h ) 20 μm in P0, 100 μm in P14, and 10 μm in P28. ( k ) 10 μm. Figure 8—source data 1. Quantification of gluteus (Gl) neuromuscular junctions (NMJs) in Isl2 +/- and Isl2 knockout (KO) mice for . Figure 8—source data 2. Quantification of tensor fasciae latae (Tfl) neuromuscular junctions (NMJs) in Isl2 +/- and Isl2 knockout (KO) mice for .

Techniques: Muscles, Knock-Out, Whisker Assay, MANN-WHITNEY

( a ) NMJs in Vl, Vm, and Ta muscles of P0 control Hb9::GFP or Isl2 knockout (KO); Hb9::GFP animals were visualized using GFP (green) and α-bungarotoxin (BTX) staining. The boxed regions on the left are shown in higher magnification on the right. Vl, vastus lateralis; Vm, vastus medialis. Scale bars, 200 μm. ( b ) Neuromuscular junctions in the psoas major, rectus femoris, vastus lateralis, tibialis anterior, and gastrocnemius muscles of Isl2 +/-; Hb9::GFP or Isl2 KO; Hb9::GFP animals at P14 were visualized using GFP (green) and BTX staining. Scale bar, 50 μm.

Journal: eLife

Article Title: Transcriptional control of motor pool formation and motor circuit connectivity by the LIM-HD protein Isl2

doi: 10.7554/eLife.84596

Figure Lengend Snippet: ( a ) NMJs in Vl, Vm, and Ta muscles of P0 control Hb9::GFP or Isl2 knockout (KO); Hb9::GFP animals were visualized using GFP (green) and α-bungarotoxin (BTX) staining. The boxed regions on the left are shown in higher magnification on the right. Vl, vastus lateralis; Vm, vastus medialis. Scale bars, 200 μm. ( b ) Neuromuscular junctions in the psoas major, rectus femoris, vastus lateralis, tibialis anterior, and gastrocnemius muscles of Isl2 +/-; Hb9::GFP or Isl2 KO; Hb9::GFP animals at P14 were visualized using GFP (green) and BTX staining. Scale bar, 50 μm.

Techniques: Muscles, Knock-Out, Staining

( a ) Tail suspension test images showing rigid wide-open posture of the hindlimbs in Isl2 mutant mice. ( b ) Footprint patterns of 3-month-old Isl2 +/- and Isl2 knockout (KO) mice. ( c ) Measurement of the stride width of forelimbs (1.56±0.06 cm for Isl2 +/- , vs. 1.73±0.06 cm for Isl2 KO, p=0.0782) and hindlimbs (2.70±0.05 cm for Isl2 +/- , vs. 3.63±0.09 cm for Isl2 KO, p<0.0001). n=5–8 animals per genotype; SEM is shown; unpaired Student’s t-test; see and source data for detailed n and statistics. ****p<0.0001, n.s.=not significant. ( d ) Gross appearance of lower limbs and dissected hindlimb samples of adult Isl2 +/- and Isl2 KO mice. ( e ) Measurement of body (9.9±0.8 g for Isl2 +/- , vs. 6.9±0.8 g for Isl2 KO, p=0.0339) and muscle weight for gluteus (GI) (67.6±12.6 mg for Isl2 +/- , vs. 34.3±2.7 mg for Isl2 KO, p=0.0316, n=5–6 muscles per group) and rectus femoris muscles (51.1±8.2 mg for Isl2 +/- , vs. 27.6±3.8 mg for Isl2 KO, p=0.0384, n=5–6 muscles per group). n=5 animals for heterozygote, n=4 animals for KO; SEM is shown; unpaired Student’s t-test; see and source data for detailed n and statistics. *p<0.05. ( f ) Representative electromyographic (EMG) recordings of Gl muscles during free-walking. ( g ) Signature of individual footsteps. (h–j) Quantification of average frequency (861±18 Hz for Isl2 +/- , vs. 619±16 Hz for Isl2 KO, p<0.0001), number of single-motor-unit potentials (80±4 peaks for Isl2 +/- , vs. 42±3 peaks for Isl2 KO, p<0.0001), and burst activity duration (0.096±0.005 s for Isl2 +/- , vs. 0.068±0.005 s for Isl2 KO, p=0.0001) in EMG recordings of Gl muscles. Three animals per group; box plots illustrate distribution with median (center line), first and third quartiles (box boundaries), and 10th-90th percentiles (whiskers); unpaired Student’s t-test; see and source data for detailed n and statistics. ****p<0.0001, ***p<0.001. Figure 9—source data 1. Measurement of stride width of forelimbs and hindlimbs in footprint analysis of 3-month-old Isl2 +/- and Isl2 knockout (KO) mice for . Measurement of body and muscle weight of the gluteus and rectus femoris muscles of Isl2 +/- and Isl2 KO mice for . Figure 9—source data 2. Quantification of the average frequency, number of single-motor-unit potentials, and burst activity duration in electromyographic (EMG) recordings of the gluteus (Gl) muscles for .

Journal: eLife

Article Title: Transcriptional control of motor pool formation and motor circuit connectivity by the LIM-HD protein Isl2

doi: 10.7554/eLife.84596

Figure Lengend Snippet: ( a ) Tail suspension test images showing rigid wide-open posture of the hindlimbs in Isl2 mutant mice. ( b ) Footprint patterns of 3-month-old Isl2 +/- and Isl2 knockout (KO) mice. ( c ) Measurement of the stride width of forelimbs (1.56±0.06 cm for Isl2 +/- , vs. 1.73±0.06 cm for Isl2 KO, p=0.0782) and hindlimbs (2.70±0.05 cm for Isl2 +/- , vs. 3.63±0.09 cm for Isl2 KO, p<0.0001). n=5–8 animals per genotype; SEM is shown; unpaired Student’s t-test; see and source data for detailed n and statistics. ****p<0.0001, n.s.=not significant. ( d ) Gross appearance of lower limbs and dissected hindlimb samples of adult Isl2 +/- and Isl2 KO mice. ( e ) Measurement of body (9.9±0.8 g for Isl2 +/- , vs. 6.9±0.8 g for Isl2 KO, p=0.0339) and muscle weight for gluteus (GI) (67.6±12.6 mg for Isl2 +/- , vs. 34.3±2.7 mg for Isl2 KO, p=0.0316, n=5–6 muscles per group) and rectus femoris muscles (51.1±8.2 mg for Isl2 +/- , vs. 27.6±3.8 mg for Isl2 KO, p=0.0384, n=5–6 muscles per group). n=5 animals for heterozygote, n=4 animals for KO; SEM is shown; unpaired Student’s t-test; see and source data for detailed n and statistics. *p<0.05. ( f ) Representative electromyographic (EMG) recordings of Gl muscles during free-walking. ( g ) Signature of individual footsteps. (h–j) Quantification of average frequency (861±18 Hz for Isl2 +/- , vs. 619±16 Hz for Isl2 KO, p<0.0001), number of single-motor-unit potentials (80±4 peaks for Isl2 +/- , vs. 42±3 peaks for Isl2 KO, p<0.0001), and burst activity duration (0.096±0.005 s for Isl2 +/- , vs. 0.068±0.005 s for Isl2 KO, p=0.0001) in EMG recordings of Gl muscles. Three animals per group; box plots illustrate distribution with median (center line), first and third quartiles (box boundaries), and 10th-90th percentiles (whiskers); unpaired Student’s t-test; see and source data for detailed n and statistics. ****p<0.0001, ***p<0.001. Figure 9—source data 1. Measurement of stride width of forelimbs and hindlimbs in footprint analysis of 3-month-old Isl2 +/- and Isl2 knockout (KO) mice for . Measurement of body and muscle weight of the gluteus and rectus femoris muscles of Isl2 +/- and Isl2 KO mice for . Figure 9—source data 2. Quantification of the average frequency, number of single-motor-unit potentials, and burst activity duration in electromyographic (EMG) recordings of the gluteus (Gl) muscles for .

Techniques: Suspension, Mutagenesis, Knock-Out, Muscles, Activity Assay

Journal: eLife

Article Title: Transcriptional control of motor pool formation and motor circuit connectivity by the LIM-HD protein Isl2

doi: 10.7554/eLife.84596

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Techniques: Sequencing, Recombinant, Plasmid Preparation, Labeling, Software

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