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full-length coding sequences including stop codon for the tfs and oncogenes  (GenScript corporation)

 
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    GenScript corporation full-length coding sequences including stop codon for the tfs and oncogenes
    A Phase contrast microscope images showing the phenotype and morphology of the cells in the course of conversion of fibroblasts to iHeps at different times points after transduction with a cocktail of three TFs HNF1A, HNF4A and FOXA3 . B Generation of highly proliferative iHep cells by transducing iHeps with two pools of liver cancer-specific oncogenic drivers, a list of xenograft experiments in nude mice that were used to test the tumorigenicity of different conditions, and mutation rates of the oncogenic drivers as reported in the COSMIC database for HCC and MYC amplification as reported in . CMT pool contains three <t>oncogenes</t> CTNNB1 T41A , MYC, and TERT, and CMT + sg TP53 pool contains the same oncogenes along with constructs for TP53 inactivation by CRISPR-Cas9. Phase contrast microscope images showing the phenotype and morphology of the cells. Oncogenes are co-transduced with fluorescent reporter mCherry for the detection of transduced cells. Oncogene transduction to fibroblasts fails to transform the cells, passaging of oncogene-expressing fibroblasts results in cellular senescence as demonstrated by β-galactosidase staining and loss of mCherry-positive oncogene-expressing cells from the fibroblast population. iHeps maintained in defined culture medium become senescent around week four of transdifferentiation although they can survive in culture for several weeks after that if not passaged. Passaging of iHeps without oncogenes results in apoptosis after few passages. Scale bar 1000 μm unless otherwise specified.
    Full Length Coding Sequences Including Stop Codon For The Tfs And Oncogenes, supplied by GenScript corporation, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/length+coding+sequence/pmc08429043-224-10-14?v=GenScript+corporation
    Average 90 stars, based on 1 article reviews
    full-length coding sequences including stop codon for the tfs and oncogenes - by Bioz Stars, 2026-07
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    1) Product Images from "Human cell transformation by combined lineage conversion and oncogene expression"

    Article Title: Human cell transformation by combined lineage conversion and oncogene expression

    Journal: Oncogene

    doi: 10.1038/s41388-021-01940-0

    A Phase contrast microscope images showing the phenotype and morphology of the cells in the course of conversion of fibroblasts to iHeps at different times points after transduction with a cocktail of three TFs HNF1A, HNF4A and FOXA3 . B Generation of highly proliferative iHep cells by transducing iHeps with two pools of liver cancer-specific oncogenic drivers, a list of xenograft experiments in nude mice that were used to test the tumorigenicity of different conditions, and mutation rates of the oncogenic drivers as reported in the COSMIC database for HCC and MYC amplification as reported in . CMT pool contains three oncogenes CTNNB1 T41A , MYC, and TERT, and CMT + sg TP53 pool contains the same oncogenes along with constructs for TP53 inactivation by CRISPR-Cas9. Phase contrast microscope images showing the phenotype and morphology of the cells. Oncogenes are co-transduced with fluorescent reporter mCherry for the detection of transduced cells. Oncogene transduction to fibroblasts fails to transform the cells, passaging of oncogene-expressing fibroblasts results in cellular senescence as demonstrated by β-galactosidase staining and loss of mCherry-positive oncogene-expressing cells from the fibroblast population. iHeps maintained in defined culture medium become senescent around week four of transdifferentiation although they can survive in culture for several weeks after that if not passaged. Passaging of iHeps without oncogenes results in apoptosis after few passages. Scale bar 1000 μm unless otherwise specified.
    Figure Legend Snippet: A Phase contrast microscope images showing the phenotype and morphology of the cells in the course of conversion of fibroblasts to iHeps at different times points after transduction with a cocktail of three TFs HNF1A, HNF4A and FOXA3 . B Generation of highly proliferative iHep cells by transducing iHeps with two pools of liver cancer-specific oncogenic drivers, a list of xenograft experiments in nude mice that were used to test the tumorigenicity of different conditions, and mutation rates of the oncogenic drivers as reported in the COSMIC database for HCC and MYC amplification as reported in . CMT pool contains three oncogenes CTNNB1 T41A , MYC, and TERT, and CMT + sg TP53 pool contains the same oncogenes along with constructs for TP53 inactivation by CRISPR-Cas9. Phase contrast microscope images showing the phenotype and morphology of the cells. Oncogenes are co-transduced with fluorescent reporter mCherry for the detection of transduced cells. Oncogene transduction to fibroblasts fails to transform the cells, passaging of oncogene-expressing fibroblasts results in cellular senescence as demonstrated by β-galactosidase staining and loss of mCherry-positive oncogene-expressing cells from the fibroblast population. iHeps maintained in defined culture medium become senescent around week four of transdifferentiation although they can survive in culture for several weeks after that if not passaged. Passaging of iHeps without oncogenes results in apoptosis after few passages. Scale bar 1000 μm unless otherwise specified.

    Techniques Used: Microscopy, Transduction, Mutagenesis, Amplification, Construct, CRISPR, Passaging, Expressing, Staining

    A Subcutaneous injection of transformed iHeps results in xenograft tumors in nude mice (tumor size of 1.5 cm ~23 weeks after xenotransplantation). Proliferative iHeps transduced with defined CMT oncogenes with TP53 inactivation (CMT + sg TP53 ) or control iHeps without oncogenes were used in the injections. B In vivo imaging of xenograft tumors ~12 weeks after implantation. Two biological replicate experiments are shown for CMT + sg TP53 cells with iHep conversion and oncogene transduction with TP53 inactivation performed in two separate human fibroblast cell lines (foreskin fibroblast [left panel] and fetal lung fibroblast [middle]) as well as proliferative CMT iHeps without TP53 inactivation (right). Fluorescence signal emitted by mCherry co-transduced with the oncogenes is detected in vivo using the Lago system (scale bar = radiance units). Control mice are injected with either fibroblasts or iHeps. C Histological analysis of CMT + sg TP53 tumor tissue harvested at 20 weeks. Hematoxylin-eosin (H&E) staining for general histology and immunohistochemical staining for Ki-67 for cell proliferation (100x magnification). Note that the appearance of the tumor is consistent with both poorly differentiated hepatic tumor or sarcoma. Differential diagnosis from sarcoma is accomplished by analysis of marker gene expression (see Figs. and ). D Analysis of chromosomal aberrations in the transformed iHeps by spectral karyotyping. CMT + sg TP53 cells were analyzed at passage 18 (early) and passage 50 (late) and CMT cells at passage 18. Fibroblasts have normal diploid karyotype (46, XY, representative spectral image on left) and transformed iHeps show aneuploidies as indicated in the figure. Early passage CMT + sg TP53 cells show two different populations with two distinct modal chromosome numbers (45, XY and 67-92, XY, representative spectral image for 45, XY on middle-left). Late passage CMT + sg TP53 cells have modal chromosome number 67-92, XY (middle-right) and CMT cells 75, XY (right). In the text box below the images, recurrent chromosomal aberrations seen in majority (>90%) of the cells are reported. E Frequencies of chromosomal alterations reported for human HCC samples [see ].
    Figure Legend Snippet: A Subcutaneous injection of transformed iHeps results in xenograft tumors in nude mice (tumor size of 1.5 cm ~23 weeks after xenotransplantation). Proliferative iHeps transduced with defined CMT oncogenes with TP53 inactivation (CMT + sg TP53 ) or control iHeps without oncogenes were used in the injections. B In vivo imaging of xenograft tumors ~12 weeks after implantation. Two biological replicate experiments are shown for CMT + sg TP53 cells with iHep conversion and oncogene transduction with TP53 inactivation performed in two separate human fibroblast cell lines (foreskin fibroblast [left panel] and fetal lung fibroblast [middle]) as well as proliferative CMT iHeps without TP53 inactivation (right). Fluorescence signal emitted by mCherry co-transduced with the oncogenes is detected in vivo using the Lago system (scale bar = radiance units). Control mice are injected with either fibroblasts or iHeps. C Histological analysis of CMT + sg TP53 tumor tissue harvested at 20 weeks. Hematoxylin-eosin (H&E) staining for general histology and immunohistochemical staining for Ki-67 for cell proliferation (100x magnification). Note that the appearance of the tumor is consistent with both poorly differentiated hepatic tumor or sarcoma. Differential diagnosis from sarcoma is accomplished by analysis of marker gene expression (see Figs. and ). D Analysis of chromosomal aberrations in the transformed iHeps by spectral karyotyping. CMT + sg TP53 cells were analyzed at passage 18 (early) and passage 50 (late) and CMT cells at passage 18. Fibroblasts have normal diploid karyotype (46, XY, representative spectral image on left) and transformed iHeps show aneuploidies as indicated in the figure. Early passage CMT + sg TP53 cells show two different populations with two distinct modal chromosome numbers (45, XY and 67-92, XY, representative spectral image for 45, XY on middle-left). Late passage CMT + sg TP53 cells have modal chromosome number 67-92, XY (middle-right) and CMT cells 75, XY (right). In the text box below the images, recurrent chromosomal aberrations seen in majority (>90%) of the cells are reported. E Frequencies of chromosomal alterations reported for human HCC samples [see ].

    Techniques Used: Injection, Transformation Assay, Transduction, Control, In Vivo Imaging, Fluorescence, In Vivo, Staining, Immunohistochemical staining, Biomarker Discovery, Marker, Gene Expression

    A Gene set enrichment analysis (GSEA) results for CMT-iHeps and CMT + sg TP53 -iHeps compared to control fibroblasts against liver cancer signature [HCC Subclass 2 ] from molecular signatures database (MSigDB). Positive normalized enrichment score (NES) reflects overrepresentation of liver cancer signature genes among the top-ranked differentially expressed genes in CMT-iHep and CMT + sg TP53 -iHep conditions compared to control fibroblasts. B Differential expression levels [log 2 (fold change)] of marker genes for fibroblasts, hepatocytes, and liver cancer in bulk RNA-seq measurements from CMT + sg TP53 -iHeps and CMT-iHeps at p20 (~22 weeks after oncogene transduction) as well as xenograft tumor from CMT + sg TP53 cells against control fibroblasts (mean ± standard error, n = 3). C IGV snapshots for promoter regions of representative genes from fibroblast markers ( MMP3 ), liver markers ( SERPINA1/α-1-antitrypsin ), and liver cancer markers ( SAA1 ) showing ATAC-seq enrichment from fibroblast and CMT + sg TP53 -iHeps. D Chromatin accessibility and CpG methylation of DNA measured using NaNoMe-seq. Cytosine methylation detected using Nanopore sequencing from CMT + sg TP53 -iHeps and control fibroblasts is shown for promoter regions of representative genes from fibroblast markers ( MMP3 ), liver markers ( SERPINA1/α-1-antitrypsin ), and liver cancer markers ( SAA1 ) using a window of TSS ± 1500 bp. GpCpH methylation (all GC sequences where the C is not part of a CG sequence also, top) reports on chromatin accessibility, whereas HpCpG methylation reports on endogenous methylation of cytosines in the CpG context. E CpG methylation detected using bisulfite-sequencing from primary human foreskin fibroblasts and from the normal adult liver [data from the Roadmap Epigenomics Consortium ]. IGV snapshots from the genomic loci corresponding to the MMP3 , SERPINA1 , and SAA1 promoters (same regions as indicated in Fig. 5D) showing methylation proportions [methylated calls/(methylated calls + unmethylated calls)] for all CpGs covered by at least 4 reads.
    Figure Legend Snippet: A Gene set enrichment analysis (GSEA) results for CMT-iHeps and CMT + sg TP53 -iHeps compared to control fibroblasts against liver cancer signature [HCC Subclass 2 ] from molecular signatures database (MSigDB). Positive normalized enrichment score (NES) reflects overrepresentation of liver cancer signature genes among the top-ranked differentially expressed genes in CMT-iHep and CMT + sg TP53 -iHep conditions compared to control fibroblasts. B Differential expression levels [log 2 (fold change)] of marker genes for fibroblasts, hepatocytes, and liver cancer in bulk RNA-seq measurements from CMT + sg TP53 -iHeps and CMT-iHeps at p20 (~22 weeks after oncogene transduction) as well as xenograft tumor from CMT + sg TP53 cells against control fibroblasts (mean ± standard error, n = 3). C IGV snapshots for promoter regions of representative genes from fibroblast markers ( MMP3 ), liver markers ( SERPINA1/α-1-antitrypsin ), and liver cancer markers ( SAA1 ) showing ATAC-seq enrichment from fibroblast and CMT + sg TP53 -iHeps. D Chromatin accessibility and CpG methylation of DNA measured using NaNoMe-seq. Cytosine methylation detected using Nanopore sequencing from CMT + sg TP53 -iHeps and control fibroblasts is shown for promoter regions of representative genes from fibroblast markers ( MMP3 ), liver markers ( SERPINA1/α-1-antitrypsin ), and liver cancer markers ( SAA1 ) using a window of TSS ± 1500 bp. GpCpH methylation (all GC sequences where the C is not part of a CG sequence also, top) reports on chromatin accessibility, whereas HpCpG methylation reports on endogenous methylation of cytosines in the CpG context. E CpG methylation detected using bisulfite-sequencing from primary human foreskin fibroblasts and from the normal adult liver [data from the Roadmap Epigenomics Consortium ]. IGV snapshots from the genomic loci corresponding to the MMP3 , SERPINA1 , and SAA1 promoters (same regions as indicated in Fig. 5D) showing methylation proportions [methylated calls/(methylated calls + unmethylated calls)] for all CpGs covered by at least 4 reads.

    Techniques Used: Control, Quantitative Proteomics, Marker, RNA Sequencing, Transduction, CpG Methylation Assay, Methylation, Nanopore Sequencing, Sequencing, Methylation Sequencing

    A Immunohistochemical analysis of xenograft tumor tissue from CMT + sg TP53 harvested at 20 weeks and xenograft tumor from the HuH7 HCC cell line. Staining for glypican-3 and arginase-1 are shown along with negative control without primary antibody (100x magnification). B (Top) Beta-galactosidase staining as a marker of cellular senescence in primary human hepatocytes (control), after transduction of CMT oncogenes, or after transduction with iHep-TFs (HNF1A, HNF4A, FOXA3) followed by CMT oncogene transduction one week later (stained three weeks after first transduction). (Middle) Beta-galactosidase staining as a marker of cellular senescence in control fibroblasts and fibroblasts transduced with CMT oncogenes and stained at p4. (Bottom) Fluorescent microscope images of induced neurons with and without transduction of neuroblastoma-specific oncogenes (at three weeks of neuronal differentiation) visualized using EGFP at ten weeks after neuronal conversion. C Schematic presentation of the molecular approach for identifying minimal determinants of tumorigenesis in specific tissues. Lineage-specific transcription factors are used to reprogram human fibroblasts to precise cellular identity (left), whose transformation by specific combinations of oncogenes (right) can then be tested. This approach combined with single-cell RNA-seq and RNA velocity analyses allows also analysis of which cell type along the stem cell to terminally differentiated cell axis (top to bottom) is susceptible for transformation.
    Figure Legend Snippet: A Immunohistochemical analysis of xenograft tumor tissue from CMT + sg TP53 harvested at 20 weeks and xenograft tumor from the HuH7 HCC cell line. Staining for glypican-3 and arginase-1 are shown along with negative control without primary antibody (100x magnification). B (Top) Beta-galactosidase staining as a marker of cellular senescence in primary human hepatocytes (control), after transduction of CMT oncogenes, or after transduction with iHep-TFs (HNF1A, HNF4A, FOXA3) followed by CMT oncogene transduction one week later (stained three weeks after first transduction). (Middle) Beta-galactosidase staining as a marker of cellular senescence in control fibroblasts and fibroblasts transduced with CMT oncogenes and stained at p4. (Bottom) Fluorescent microscope images of induced neurons with and without transduction of neuroblastoma-specific oncogenes (at three weeks of neuronal differentiation) visualized using EGFP at ten weeks after neuronal conversion. C Schematic presentation of the molecular approach for identifying minimal determinants of tumorigenesis in specific tissues. Lineage-specific transcription factors are used to reprogram human fibroblasts to precise cellular identity (left), whose transformation by specific combinations of oncogenes (right) can then be tested. This approach combined with single-cell RNA-seq and RNA velocity analyses allows also analysis of which cell type along the stem cell to terminally differentiated cell axis (top to bottom) is susceptible for transformation.

    Techniques Used: Immunohistochemical staining, Staining, Negative Control, Marker, Control, Transduction, Microscopy, Transformation Assay, RNA Sequencing

    A , B t-SNE plots of 3,500 single cells from fibroblasts, iHeps at one to three weeks after iHep induction, iHeps transduced with CMT oncogenes at one week and harvested for scRNA-seq two weeks later, and fibroblasts transduced with CMT oncogenes and harvested at one and three weeks. Cells are colored by sample ( A ), and distinct clusters ( B ) based on their expression profiles with sample collection time points indicated. C Principal component analysis (PCA) projection of single cells from control fibroblasts, iHeps at one to three weeks after iHep induction, and CMT-iHeps two weeks after oncogenes shown with velocity field with the observed states of the cells shown as circles and the extrapolated future states shown with arrows for the first two principal components. Cells are colored by cluster identities corresponding to Fig. 4B. D Relative expression of the genes from the Notch signaling pathway (panel on the right) across pseudotime in the single-cell RNA-seq data from control fibroblasts, iHeps at one to three weeks after iHep induction, and CMT-iHeps two weeks after oncogenes (the expression of a gene in a particular cell relative to the average expression of that gene across all cells). Relative expression of the senescence marker genes (panel on the left) from control fibroblasts and fibroblasts transduced with CMT oncogenes and harvested at one and three weeks after transduction. Color codes illustrating sample and cluster identities correspond to the colors in Fig. 4A, B, respectively. E Expression levels [log 2 (transcripts per million, tpm)] for LGR5 as well as lentiviral and endogenous HNF4A, TERT , and CTNNB1 in bulk RNA-seq measurements from control fibroblasts, iHeps at four weeks of differentiation, CMT + sg TP53 -iHeps at two and 22 weeks after oncogene transduction, xenograft tumor from CMT + sg TP53 cells, and from liver cancer cell lines HepG2 and HuH7 (mean ± standard error, n = 3). Nanopore sequencing was performed from the CMT + sg TP53 cells at 22 weeks after oncogene transduction as indicated in the figure and used for identifying the genomic insertions of the lentiviral constructs (Supplementary Table ).
    Figure Legend Snippet: A , B t-SNE plots of 3,500 single cells from fibroblasts, iHeps at one to three weeks after iHep induction, iHeps transduced with CMT oncogenes at one week and harvested for scRNA-seq two weeks later, and fibroblasts transduced with CMT oncogenes and harvested at one and three weeks. Cells are colored by sample ( A ), and distinct clusters ( B ) based on their expression profiles with sample collection time points indicated. C Principal component analysis (PCA) projection of single cells from control fibroblasts, iHeps at one to three weeks after iHep induction, and CMT-iHeps two weeks after oncogenes shown with velocity field with the observed states of the cells shown as circles and the extrapolated future states shown with arrows for the first two principal components. Cells are colored by cluster identities corresponding to Fig. 4B. D Relative expression of the genes from the Notch signaling pathway (panel on the right) across pseudotime in the single-cell RNA-seq data from control fibroblasts, iHeps at one to three weeks after iHep induction, and CMT-iHeps two weeks after oncogenes (the expression of a gene in a particular cell relative to the average expression of that gene across all cells). Relative expression of the senescence marker genes (panel on the left) from control fibroblasts and fibroblasts transduced with CMT oncogenes and harvested at one and three weeks after transduction. Color codes illustrating sample and cluster identities correspond to the colors in Fig. 4A, B, respectively. E Expression levels [log 2 (transcripts per million, tpm)] for LGR5 as well as lentiviral and endogenous HNF4A, TERT , and CTNNB1 in bulk RNA-seq measurements from control fibroblasts, iHeps at four weeks of differentiation, CMT + sg TP53 -iHeps at two and 22 weeks after oncogene transduction, xenograft tumor from CMT + sg TP53 cells, and from liver cancer cell lines HepG2 and HuH7 (mean ± standard error, n = 3). Nanopore sequencing was performed from the CMT + sg TP53 cells at 22 weeks after oncogene transduction as indicated in the figure and used for identifying the genomic insertions of the lentiviral constructs (Supplementary Table ).

    Techniques Used: Transduction, Expressing, Control, RNA Sequencing, Marker, Nanopore Sequencing, Construct



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    Image Search Results


    Silencing of GmMEKK2 by virus‐induced gene silencing (VIGS) increased soybean mosaic virus (SMV) susceptibility. (A) Efficiency of GmMEKK2 silencing in empty vector control (EV) and GmMEKK2 ‐silenced mekk2 i1 and mekk2 i2 plants at 0, 7, 14 and 21 days post‐inoculation (dpi). (B) Phenotypes of soybean after SMV infection: EV and GmMEKK2 ‐silenced lines generated using VIGS. Images were taken at 21 dpi. (C) Disease indices of plants at 21 dpi. Lowercase letters denote statistically significant differences among groups at the same time point ( p < 0.05, one‐way ANOVA with Duncan's test). (D) Relative SMV accumulation in top new leaves of EV and GmMEKK2 ‐silenced plants at 7, 14 and 21 dpi, quantified by reverse transcription‐quantitative PCR using SMV coat protein‐specific primers.

    Journal: Molecular Plant Pathology

    Article Title: GmMEKK2 Disrupts the MKK1 /2– MPK4 Cascade to Amplify Immune Signalling and Confer Enhanced Resistance to Soybean Mosaic Virus

    doi: 10.1111/mpp.70184

    Figure Lengend Snippet: Silencing of GmMEKK2 by virus‐induced gene silencing (VIGS) increased soybean mosaic virus (SMV) susceptibility. (A) Efficiency of GmMEKK2 silencing in empty vector control (EV) and GmMEKK2 ‐silenced mekk2 i1 and mekk2 i2 plants at 0, 7, 14 and 21 days post‐inoculation (dpi). (B) Phenotypes of soybean after SMV infection: EV and GmMEKK2 ‐silenced lines generated using VIGS. Images were taken at 21 dpi. (C) Disease indices of plants at 21 dpi. Lowercase letters denote statistically significant differences among groups at the same time point ( p < 0.05, one‐way ANOVA with Duncan's test). (D) Relative SMV accumulation in top new leaves of EV and GmMEKK2 ‐silenced plants at 7, 14 and 21 dpi, quantified by reverse transcription‐quantitative PCR using SMV coat protein‐specific primers.

    Article Snippet: The GmMEKK2 full‐length coding DNA sequence (CDS) was inserted into pDONOR221 (Invitrogen) and then transferred to a pB7FWG2 vector via an LR recombination reaction in the Gateway system.

    Techniques: Virus, Plasmid Preparation, Control, Infection, Generated, Reverse Transcription, Real-time Polymerase Chain Reaction

    Overexpression of GmMEKK2 improved soybean mosaic virus (SMV) resistance in soybean. (A) Infection symptoms on soybean leaves after SMV inoculation. NT, nontransgenic plants; ZMP1, 3, 6 and 7 indicate GmMEKK2 ‐overexpression lines 1, 3, 6 and 7, respectively. (B) Disease indices of NT and each GmMEKK2 ‐overexpression line. The disease index was investigated at 21 days post‐SMV‐inoculation. (C) Quantification of SMV content in soybean leaves. SMV‐susceptible line 1138‐2 was used as a positive control. (D) The GmMEKK2 expression pattern in NT plants after SMV inoculation. (E) Comparison of yield traits between NT and overexpression plants after SMV infection. Mock‐inoculated plants served as the control. Values labelled with different lowercase letters (a–e) are significantly different at p < 0.05 as determined by Duncan's test.

    Journal: Molecular Plant Pathology

    Article Title: GmMEKK2 Disrupts the MKK1 /2– MPK4 Cascade to Amplify Immune Signalling and Confer Enhanced Resistance to Soybean Mosaic Virus

    doi: 10.1111/mpp.70184

    Figure Lengend Snippet: Overexpression of GmMEKK2 improved soybean mosaic virus (SMV) resistance in soybean. (A) Infection symptoms on soybean leaves after SMV inoculation. NT, nontransgenic plants; ZMP1, 3, 6 and 7 indicate GmMEKK2 ‐overexpression lines 1, 3, 6 and 7, respectively. (B) Disease indices of NT and each GmMEKK2 ‐overexpression line. The disease index was investigated at 21 days post‐SMV‐inoculation. (C) Quantification of SMV content in soybean leaves. SMV‐susceptible line 1138‐2 was used as a positive control. (D) The GmMEKK2 expression pattern in NT plants after SMV inoculation. (E) Comparison of yield traits between NT and overexpression plants after SMV infection. Mock‐inoculated plants served as the control. Values labelled with different lowercase letters (a–e) are significantly different at p < 0.05 as determined by Duncan's test.

    Article Snippet: The GmMEKK2 full‐length coding DNA sequence (CDS) was inserted into pDONOR221 (Invitrogen) and then transferred to a pB7FWG2 vector via an LR recombination reaction in the Gateway system.

    Techniques: Over Expression, Virus, Infection, Positive Control, Expressing, Comparison, Control

    Expression profiles of key differentially expressed genes (DEGs) between nontransgenic (NT) and GmMEKK2 ‐overexpression lines (ZMP) involved in the reactive oxygen species (ROS)‐ and salicylic acid (SA)‐related pathways. (A) KEGG enrichment analysis of DEGs between NT and ZMP plants. Left: NT_CK versus ZMP_CK (uninfected controls); Right: NT_7d versus ZMP_7d (7 days post‐SMV‐inoculation [dpi]). Points represent enriched pathways, with size indicating gene count and colour reflecting −log 10 (adjusted p ‐value). Red arrows highlight defence‐related pathways. (B) Expression dynamics of key components among MAPK, plant hormone signalling and plant–pathogen interaction pathways. Schematic depicts signal transduction from apoplast to cytoplasm, including Ca 2+ sensors (CNGCs and CDPKs), ROS producers (Rbohs) and SA‐induced defence protein (PR1). Heatmaps show expression levels across conditions (NT and ZMP at 0, 7 and 14 dpi), with gene IDs labelled.

    Journal: Molecular Plant Pathology

    Article Title: GmMEKK2 Disrupts the MKK1 /2– MPK4 Cascade to Amplify Immune Signalling and Confer Enhanced Resistance to Soybean Mosaic Virus

    doi: 10.1111/mpp.70184

    Figure Lengend Snippet: Expression profiles of key differentially expressed genes (DEGs) between nontransgenic (NT) and GmMEKK2 ‐overexpression lines (ZMP) involved in the reactive oxygen species (ROS)‐ and salicylic acid (SA)‐related pathways. (A) KEGG enrichment analysis of DEGs between NT and ZMP plants. Left: NT_CK versus ZMP_CK (uninfected controls); Right: NT_7d versus ZMP_7d (7 days post‐SMV‐inoculation [dpi]). Points represent enriched pathways, with size indicating gene count and colour reflecting −log 10 (adjusted p ‐value). Red arrows highlight defence‐related pathways. (B) Expression dynamics of key components among MAPK, plant hormone signalling and plant–pathogen interaction pathways. Schematic depicts signal transduction from apoplast to cytoplasm, including Ca 2+ sensors (CNGCs and CDPKs), ROS producers (Rbohs) and SA‐induced defence protein (PR1). Heatmaps show expression levels across conditions (NT and ZMP at 0, 7 and 14 dpi), with gene IDs labelled.

    Article Snippet: The GmMEKK2 full‐length coding DNA sequence (CDS) was inserted into pDONOR221 (Invitrogen) and then transferred to a pB7FWG2 vector via an LR recombination reaction in the Gateway system.

    Techniques: Expressing, Over Expression, Transduction

    Kinase activity of GmMEKK2 is dispensable for its function in mediating defence signalling. (A–E) Relative expression levels of (A) GmMKK1 , (B) GmMPK4A , (C) GmMPK13‐like , (D) GmSUMM2 and (E) GmCRCK3 in nontransgenic control (NT), GmMEKK2 ‐overexpression lines (ZMP1, ZMP3 and ZMP7), empty vector control (EV) and GmMEKK2‐ silenced lines ( mekk2 i1 and mekk2 i2 ). Lowercase letters denote significant differences at p < 0.05 as determined by one‐way ANOVA with Duncan's test. (F) Domain architecture of GmMEKK2 highlighting the kinase domain (6–264 amino acids) and ATP‐binding site (K36). Autophosphorylation of GmMEKK2 was assessed by immunoblotting with α‐pSer/Thr antibody. Recombinant proteins GmMEKK1‐FLAG and GmMEKK1 K321M ‐FLAG were used as positive and negative controls, respectively. Coomassie brilliant blue staining validated the equal loading of recombinant proteins. (G) Yeast two‐hybrid analysis of GmMEKK2 interaction with GmMKK1, GmMPK4A and GmMPK13‐like. Transformants expressing pGADT7 and pGBKT7 constructs were grown on SD/−Leu/−Trp (control) and SD/−Leu/−Trp/−Ade/−His (selection) media. (H–J) Glutathione S‐transferase (GST) pull‐down assays with anti‐His and anti‐GST antibodies demonstrating direct binding between GST‐GmMEKK2 and (H) GmMKK1‐His, (I) GmMPK4A‐His and (J) GmMPK13‐like‐His.

    Journal: Molecular Plant Pathology

    Article Title: GmMEKK2 Disrupts the MKK1 /2– MPK4 Cascade to Amplify Immune Signalling and Confer Enhanced Resistance to Soybean Mosaic Virus

    doi: 10.1111/mpp.70184

    Figure Lengend Snippet: Kinase activity of GmMEKK2 is dispensable for its function in mediating defence signalling. (A–E) Relative expression levels of (A) GmMKK1 , (B) GmMPK4A , (C) GmMPK13‐like , (D) GmSUMM2 and (E) GmCRCK3 in nontransgenic control (NT), GmMEKK2 ‐overexpression lines (ZMP1, ZMP3 and ZMP7), empty vector control (EV) and GmMEKK2‐ silenced lines ( mekk2 i1 and mekk2 i2 ). Lowercase letters denote significant differences at p < 0.05 as determined by one‐way ANOVA with Duncan's test. (F) Domain architecture of GmMEKK2 highlighting the kinase domain (6–264 amino acids) and ATP‐binding site (K36). Autophosphorylation of GmMEKK2 was assessed by immunoblotting with α‐pSer/Thr antibody. Recombinant proteins GmMEKK1‐FLAG and GmMEKK1 K321M ‐FLAG were used as positive and negative controls, respectively. Coomassie brilliant blue staining validated the equal loading of recombinant proteins. (G) Yeast two‐hybrid analysis of GmMEKK2 interaction with GmMKK1, GmMPK4A and GmMPK13‐like. Transformants expressing pGADT7 and pGBKT7 constructs were grown on SD/−Leu/−Trp (control) and SD/−Leu/−Trp/−Ade/−His (selection) media. (H–J) Glutathione S‐transferase (GST) pull‐down assays with anti‐His and anti‐GST antibodies demonstrating direct binding between GST‐GmMEKK2 and (H) GmMKK1‐His, (I) GmMPK4A‐His and (J) GmMPK13‐like‐His.

    Article Snippet: The GmMEKK2 full‐length coding DNA sequence (CDS) was inserted into pDONOR221 (Invitrogen) and then transferred to a pB7FWG2 vector via an LR recombination reaction in the Gateway system.

    Techniques: Activity Assay, Expressing, Control, Over Expression, Plasmid Preparation, Binding Assay, Western Blot, Recombinant, Staining, Construct, Selection

    GmMEKK2 promotes the immune response induced by salicylic acid (SA). (A) Contents of free (SA) and bound salicylic acid (SAG) in nontransgenic (NT) and GmMEKK2 ‐overexpression (ZMP) lines. (B) GmMEKK2 expression in NT plants after exogenous hormone treatments. ETH, ethylene; ABA, abscisic acid (C–H) Expression of pivotal genes in the SA signalling pathway in NT, GmMEKK2 ‐overexpression and GmMEKK2 ‐silenced ( mekk2 i1 and mekk2 i2 ) plants at 7 days post‐inoculation. EV, empty vector. Values labelled with different lowercase letters (a–c) are significantly different at p < 0.05 as determined by Duncan's test.

    Journal: Molecular Plant Pathology

    Article Title: GmMEKK2 Disrupts the MKK1 /2– MPK4 Cascade to Amplify Immune Signalling and Confer Enhanced Resistance to Soybean Mosaic Virus

    doi: 10.1111/mpp.70184

    Figure Lengend Snippet: GmMEKK2 promotes the immune response induced by salicylic acid (SA). (A) Contents of free (SA) and bound salicylic acid (SAG) in nontransgenic (NT) and GmMEKK2 ‐overexpression (ZMP) lines. (B) GmMEKK2 expression in NT plants after exogenous hormone treatments. ETH, ethylene; ABA, abscisic acid (C–H) Expression of pivotal genes in the SA signalling pathway in NT, GmMEKK2 ‐overexpression and GmMEKK2 ‐silenced ( mekk2 i1 and mekk2 i2 ) plants at 7 days post‐inoculation. EV, empty vector. Values labelled with different lowercase letters (a–c) are significantly different at p < 0.05 as determined by Duncan's test.

    Article Snippet: The GmMEKK2 full‐length coding DNA sequence (CDS) was inserted into pDONOR221 (Invitrogen) and then transferred to a pB7FWG2 vector via an LR recombination reaction in the Gateway system.

    Techniques: Over Expression, Expressing, Plasmid Preparation

    GmMEKK2 is involved in the regulation of reactive oxygen species homeostasis in soybean. (A, B) H 2 O 2 and O 2− levels in leaves were detected at 7 days post‐inoculation (dpi) using 3,3′‐diaminobenzidine (DAB) and nitroblue tetrazolium (NBT) staining, respectively. The mock‐inoculated leaves were sampled as controls. (C–G) Trends in the gene expression of antioxidases were measured after soybean mosaic virus (SMV) infection. CK, noninoculated control (H–J) Antioxidase activities were measured. POD, peroxidase; CAT, catalase; SOD, superoxide dismutase. The statistical analysis was independently performed for GmMEKK2 ‐overexpression lines ZMP1, ZMP3 and ZMP7, and gene‐silenced lines mekk2 i1 , mekk2 i2 and nontransgenic (NT) plants at each stage. Values labelled with different lowercase letters are significantly different at p < 0.05 as determined by Duncan's test.

    Journal: Molecular Plant Pathology

    Article Title: GmMEKK2 Disrupts the MKK1 /2– MPK4 Cascade to Amplify Immune Signalling and Confer Enhanced Resistance to Soybean Mosaic Virus

    doi: 10.1111/mpp.70184

    Figure Lengend Snippet: GmMEKK2 is involved in the regulation of reactive oxygen species homeostasis in soybean. (A, B) H 2 O 2 and O 2− levels in leaves were detected at 7 days post‐inoculation (dpi) using 3,3′‐diaminobenzidine (DAB) and nitroblue tetrazolium (NBT) staining, respectively. The mock‐inoculated leaves were sampled as controls. (C–G) Trends in the gene expression of antioxidases were measured after soybean mosaic virus (SMV) infection. CK, noninoculated control (H–J) Antioxidase activities were measured. POD, peroxidase; CAT, catalase; SOD, superoxide dismutase. The statistical analysis was independently performed for GmMEKK2 ‐overexpression lines ZMP1, ZMP3 and ZMP7, and gene‐silenced lines mekk2 i1 , mekk2 i2 and nontransgenic (NT) plants at each stage. Values labelled with different lowercase letters are significantly different at p < 0.05 as determined by Duncan's test.

    Article Snippet: The GmMEKK2 full‐length coding DNA sequence (CDS) was inserted into pDONOR221 (Invitrogen) and then transferred to a pB7FWG2 vector via an LR recombination reaction in the Gateway system.

    Techniques: Staining, Gene Expression, Virus, Infection, Control, Over Expression

    Molecular mechanisms underlying the GmMEKK2‐mediated regulation of soybean mosaic virus (SMV) resistance in soybean. (A) Phenotype and regulatory mechanism of GmMEKK2 ‐overexpression plants under SMV inoculation. Left: GmMEKK2 ‐overexpression plants (ZMP) show no visible SMV symptoms with autoimmunity phenotype such as leaf yellowing. Right: In ZMP plants, GmMEKK2 (orange ellipses) interacts with GmMKK1 and GmMPK4A, blocking the phosphorylation (letter P in a blue circle) of the GmMEKK1‐GmMKK1‐GmMPK4A cascade. This inhibition represses (cross in a red circle) WRKY transcription factors and leads to non‐phosphorylated CRCK3 releasing SUMM2. This then triggers defence responses such as salicylic acid (SA)‐induced gene expression and basal reactive oxygen species (ROS) accumulation. The elevated ROS constitutivly results in autoimmunity in ZMP plants. (B) Left: Nontransgenic (NT) plants exhibit severe SMV symptoms such as mosaic leaves and mottled pods. Right: In NT plants, GmMEKK2 expression is low, so the GmMEKK1‐GmMKK1‐GmMPK4A cascade remains active. GmMPK4A phosphorylates CRCK3, which binds with and represses SUMM2. This suppresses defence responses, and leads to a ROS burst.

    Journal: Molecular Plant Pathology

    Article Title: GmMEKK2 Disrupts the MKK1 /2– MPK4 Cascade to Amplify Immune Signalling and Confer Enhanced Resistance to Soybean Mosaic Virus

    doi: 10.1111/mpp.70184

    Figure Lengend Snippet: Molecular mechanisms underlying the GmMEKK2‐mediated regulation of soybean mosaic virus (SMV) resistance in soybean. (A) Phenotype and regulatory mechanism of GmMEKK2 ‐overexpression plants under SMV inoculation. Left: GmMEKK2 ‐overexpression plants (ZMP) show no visible SMV symptoms with autoimmunity phenotype such as leaf yellowing. Right: In ZMP plants, GmMEKK2 (orange ellipses) interacts with GmMKK1 and GmMPK4A, blocking the phosphorylation (letter P in a blue circle) of the GmMEKK1‐GmMKK1‐GmMPK4A cascade. This inhibition represses (cross in a red circle) WRKY transcription factors and leads to non‐phosphorylated CRCK3 releasing SUMM2. This then triggers defence responses such as salicylic acid (SA)‐induced gene expression and basal reactive oxygen species (ROS) accumulation. The elevated ROS constitutivly results in autoimmunity in ZMP plants. (B) Left: Nontransgenic (NT) plants exhibit severe SMV symptoms such as mosaic leaves and mottled pods. Right: In NT plants, GmMEKK2 expression is low, so the GmMEKK1‐GmMKK1‐GmMPK4A cascade remains active. GmMPK4A phosphorylates CRCK3, which binds with and represses SUMM2. This suppresses defence responses, and leads to a ROS burst.

    Article Snippet: The GmMEKK2 full‐length coding DNA sequence (CDS) was inserted into pDONOR221 (Invitrogen) and then transferred to a pB7FWG2 vector via an LR recombination reaction in the Gateway system.

    Techniques: Virus, Over Expression, Blocking Assay, Phospho-proteomics, Inhibition, Gene Expression, Expressing