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human crispr ko pooled library  (Addgene inc)


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    Addgene inc human crispr ko pooled library
    ACE2-independent binding of the Omicron RBD to cell surface HS. ( A ) <t>CRISPR</t> KO library screening scheme to identify Omicron RBD binding molecules expressed <t>on</t> <t>HEK293T</t> cells. ( B ) Binding of CRISPR KO library-transduced HEK293T cells with (red line) or without (shaded gray) Omicron RBD-Fc, before and after sorting. ( C ) Number of sgRNA sequences identified in Omicron RBD-Fc non-binding cells after sorting. Red: GAG-synthesis-related genes; black: other expressed genes; gray: non-expressed genes in HEK293T cells. ( D ) HS biosynthetic pathway highlighting SLC35B2 and B3GAT3. PAPS, 3'-phosphoadenosine-5'-phosphosulfate; Xyl, xylose; Gal, galactose; GlcNAc, N-acetylglucosamine; GlcA, glucuronic acid; IdoA, iduronic acid. ( E ) Binding of BA.1 RBD-Fc, anti-HS Ab, or anti-CS Ab to mock (black line), or SLC35B2 or B3GAT3 KO (red line) HEK293T cells. ( F ) Binding of WT or BA.1 RBD-Fc, PILRα-Fc, anti-HS Ab, or anti-CS Ab to ACE2 KO HEK293T cells pretreated with (+) or without (–) heparinase or chondroitinase. ( G ) Binding of WT or BA.1 RBD-Fc to HEK293T cells at different heparin concentrations. RBD-Fc binding was normalized to binding in the absence of heparin. ( H ) Immunofluorescence of human nasal tissue with anti-HS Ab and 4', 6-diamidino-2-phenylindole (DAPI). Scale bar, 200 µm. ( I ) Binding of WT or BA.1 RBD-Fc, anti-ACE2 Ab, or anti-HS Ab to cell lines. Data are mean ± SEM of three to four technical replicates. Statistical analysis was performed using two-way ANOVA with Sidak’s multiple comparison tests in panel F ; * P < 0.05, ** P < 0.01, and **** P < 0.0001; ns, not significant. Data are representative of two to three independent experiments.
    Human Crispr Ko Pooled Library, supplied by Addgene inc, used in various techniques. Bioz Stars score: 96/100, based on 224 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/human+crispr+ko+pooled+library+gecko+v2/Human+CRISPR+Knockout+Pooled+Library+(GeCKO+v2)+(Pooled+Library+%231000000048%2C+%231000000049)/pmc12345153-254-12-19
    Average 96 stars, based on 224 article reviews
    human crispr ko pooled library - by Bioz Stars, 2026-09
    96/100 stars

    Images

    1) Product Images from "Evolutionary dynamics of heparan sulfate utilization by SARS-CoV-2"

    Article Title: Evolutionary dynamics of heparan sulfate utilization by SARS-CoV-2

    Journal: mBio

    doi: 10.1128/mbio.01303-25

    ACE2-independent binding of the Omicron RBD to cell surface HS. ( A ) CRISPR KO library screening scheme to identify Omicron RBD binding molecules expressed on HEK293T cells. ( B ) Binding of CRISPR KO library-transduced HEK293T cells with (red line) or without (shaded gray) Omicron RBD-Fc, before and after sorting. ( C ) Number of sgRNA sequences identified in Omicron RBD-Fc non-binding cells after sorting. Red: GAG-synthesis-related genes; black: other expressed genes; gray: non-expressed genes in HEK293T cells. ( D ) HS biosynthetic pathway highlighting SLC35B2 and B3GAT3. PAPS, 3'-phosphoadenosine-5'-phosphosulfate; Xyl, xylose; Gal, galactose; GlcNAc, N-acetylglucosamine; GlcA, glucuronic acid; IdoA, iduronic acid. ( E ) Binding of BA.1 RBD-Fc, anti-HS Ab, or anti-CS Ab to mock (black line), or SLC35B2 or B3GAT3 KO (red line) HEK293T cells. ( F ) Binding of WT or BA.1 RBD-Fc, PILRα-Fc, anti-HS Ab, or anti-CS Ab to ACE2 KO HEK293T cells pretreated with (+) or without (–) heparinase or chondroitinase. ( G ) Binding of WT or BA.1 RBD-Fc to HEK293T cells at different heparin concentrations. RBD-Fc binding was normalized to binding in the absence of heparin. ( H ) Immunofluorescence of human nasal tissue with anti-HS Ab and 4', 6-diamidino-2-phenylindole (DAPI). Scale bar, 200 µm. ( I ) Binding of WT or BA.1 RBD-Fc, anti-ACE2 Ab, or anti-HS Ab to cell lines. Data are mean ± SEM of three to four technical replicates. Statistical analysis was performed using two-way ANOVA with Sidak’s multiple comparison tests in panel F ; * P < 0.05, ** P < 0.01, and **** P < 0.0001; ns, not significant. Data are representative of two to three independent experiments.
    Figure Legend Snippet: ACE2-independent binding of the Omicron RBD to cell surface HS. ( A ) CRISPR KO library screening scheme to identify Omicron RBD binding molecules expressed on HEK293T cells. ( B ) Binding of CRISPR KO library-transduced HEK293T cells with (red line) or without (shaded gray) Omicron RBD-Fc, before and after sorting. ( C ) Number of sgRNA sequences identified in Omicron RBD-Fc non-binding cells after sorting. Red: GAG-synthesis-related genes; black: other expressed genes; gray: non-expressed genes in HEK293T cells. ( D ) HS biosynthetic pathway highlighting SLC35B2 and B3GAT3. PAPS, 3'-phosphoadenosine-5'-phosphosulfate; Xyl, xylose; Gal, galactose; GlcNAc, N-acetylglucosamine; GlcA, glucuronic acid; IdoA, iduronic acid. ( E ) Binding of BA.1 RBD-Fc, anti-HS Ab, or anti-CS Ab to mock (black line), or SLC35B2 or B3GAT3 KO (red line) HEK293T cells. ( F ) Binding of WT or BA.1 RBD-Fc, PILRα-Fc, anti-HS Ab, or anti-CS Ab to ACE2 KO HEK293T cells pretreated with (+) or without (–) heparinase or chondroitinase. ( G ) Binding of WT or BA.1 RBD-Fc to HEK293T cells at different heparin concentrations. RBD-Fc binding was normalized to binding in the absence of heparin. ( H ) Immunofluorescence of human nasal tissue with anti-HS Ab and 4', 6-diamidino-2-phenylindole (DAPI). Scale bar, 200 µm. ( I ) Binding of WT or BA.1 RBD-Fc, anti-ACE2 Ab, or anti-HS Ab to cell lines. Data are mean ± SEM of three to four technical replicates. Statistical analysis was performed using two-way ANOVA with Sidak’s multiple comparison tests in panel F ; * P < 0.05, ** P < 0.01, and **** P < 0.0001; ns, not significant. Data are representative of two to three independent experiments.

    Techniques Used: Binding Assay, CRISPR, Library Screening, Immunofluorescence, Comparison

    Related Articles

    CRISPR:

    Article Title: Identification of BLNK and BTK as mediators of rituximab-induced programmed cell death by CRISPR screens in GCB-subtype diffuse large B-cell lymphoma.
    Article Snippet: OCI-Ly-7 cells were screened using the GeCKOv2 genome-wide library, essentially as previously described [37], at three different conditions: (a) medium containing human serum (HS; mock), (b) medium containing 10 μg mL 1 RTX (MabThera ; Roche, Copenhagen, Denmark), one-time administration of HS [exposure to CDC conditions, SEC (RTX-SEC); 14 days], and (c) medium with 10 μg mL 1 RTX increased to 25 μg mL 1 at day 16 and with repeated re-administration of HS [repeated exposure to CDC conditions, REC (RTX-REC); 21 days]. .. Human GeCKOv2 CRISPR KO pooled library was a gift from Feng Zhang (Addgene #1000000049, Watertown, MA, USA). ..

    Article Title: Identification of two lipid phosphatases that regulate sphingosine-1-phosphate cellular uptake and recycling
    Article Snippet: Hygromycin B, puromycin, blasticidin, G418, and Lipofectamine 3000 reagent were purchased from Thermo Fisher Scientific (Waltham, MA). .. Human genome-wide CRISPR/Cas9 KO (GeCKOv2) CRISPR KO pooled library was a gift from Feng Zhang (Addgene, Watertown, MA; Cat# 1000000049), and the lentiviral packaging of the library was accomplished by Vector Builder (Chicago, IL). .. S1P was purchased from Avanti Polar Lipids (Alabaster, AL), Shiga toxin 2 from Escherichia coli was obtained from List Labs (Campbell, CA), and myriocin was obtained from Cayman Chemical (Ann Arbor, MI).

    Article Title: Genome-wide screen based on 2DG activated NLRP3 inflammasome reveals the priming signal of TLR2/4 to IKKβ but not IKKα.
    Article Snippet: NLRP3 inflammasome activation is a pivotal area of research in innate immunity, yet the precise priming and activation signal remain unclear.. In this study, we demonstrate that glycolysis inhibitor 2-Deoxy-D-glucose (2DG) triggers NLRP3-driven pyroptosis in human leukemia monocyte THP-1 cells by interfering glycosylation rather than glycolysis, which occurs independent of potassium efflux but requires the involvement of glycolysis rate-limiting enzyme PFKP.. Using a CRISPRCas9 mediated large-scale screen, with 2DG as a new tool for probing NLRP3 activation, we identified that TLR2, rather than TLR4, initiates a rapid and robust priming signal for NLRP3 inflammasome activation.

    Article Title: Evolutionary dynamics of heparan sulfate utilization by SARS-CoV-2.
    Article Snippet: .. CRISPR KO library-transduced HEK293T cells were generated by lentivirus-mediated transduction using the Human CRISPR KO Pooled Library (GeCKO v2; Addgene, 1000000048). ..

    Article Title: Evolutionary dynamics of heparan sulfate utilization by SARS-CoV-2
    Article Snippet: .. CRISPR KO library-transduced HEK293T cells were generated by lentivirus-mediated transduction using the Human CRISPR KO Pooled Library (GeCKO v2; Addgene, 1000000048). ..

    Article Title: PP6 regulation of Aurora A–TPX2 limits NDC80 phosphorylation and mitotic spindle size
    Article Snippet: Transgene expression was induced by addition of 1 μg/ml doxycycline (D9891; Merck) to the culture medium for minimum of 24 h. .. Human genome targeting CRISPR KO (GeCKO) v2 lentiviral pooled libraries (A and B libraries) were purchased from Addgene and amplified according to a published protocol ( ). ..

    Article Title: Genome-wide CRISPR screen reveals CLPTM1L as a lipid scramblase required for efficient glycosylphosphatidylinositol biosynthesis
    Article Snippet: .. Human GeCKOv2 CRISPR KO pooled library (Pooled Library #1000000048), pX330-U6-Chimeric_BB-CBh-hSpCas9 (Addgene plasmid #42230), and lentiCRISPR v2 (Addgene plasmid #52961) were gifts from Feng Zhang, Broad Institute of MIT and Harvard, Cambridge, MA ( , ). pX330-EGFP plasmid was generated from pX330-U6-Chimeric_BB-CBh-hSpCas9 ( ). ..

    Article Title: Genome-wide CRISPR screen reveals CLPTM1L as a lipid scramblase required for efficient glycosylphosphatidylinositol biosynthesis.
    Article Snippet: .. Human GeCKOv2 CRISPR KO pooled library (Pooled Library #1000000048), pX330-U6-Chimeric_BB-CBh-hSpCas9 (Addgene plasmid #42230), and lentiCRISPR v2 (Addgene plasmid #52961) were gifts from Feng Zhang, Broad Institute of MIT and Harvard, Cambridge, MA (15, 61). pX330EGFP plasmid was generated from pX330-U6-Chimeric_BB-CBh-hSpCas9 (62). ..

    Genome Wide:

    Article Title: Identification of two lipid phosphatases that regulate sphingosine-1-phosphate cellular uptake and recycling
    Article Snippet: Hygromycin B, puromycin, blasticidin, G418, and Lipofectamine 3000 reagent were purchased from Thermo Fisher Scientific (Waltham, MA). .. Human genome-wide CRISPR/Cas9 KO (GeCKOv2) CRISPR KO pooled library was a gift from Feng Zhang (Addgene, Watertown, MA; Cat# 1000000049), and the lentiviral packaging of the library was accomplished by Vector Builder (Chicago, IL). .. S1P was purchased from Avanti Polar Lipids (Alabaster, AL), Shiga toxin 2 from Escherichia coli was obtained from List Labs (Campbell, CA), and myriocin was obtained from Cayman Chemical (Ann Arbor, MI).

    Article Title: Genome-wide screen based on 2DG activated NLRP3 inflammasome reveals the priming signal of TLR2/4 to IKKβ but not IKKα.
    Article Snippet: NLRP3 inflammasome activation is a pivotal area of research in innate immunity, yet the precise priming and activation signal remain unclear.. In this study, we demonstrate that glycolysis inhibitor 2-Deoxy-D-glucose (2DG) triggers NLRP3-driven pyroptosis in human leukemia monocyte THP-1 cells by interfering glycosylation rather than glycolysis, which occurs independent of potassium efflux but requires the involvement of glycolysis rate-limiting enzyme PFKP.. Using a CRISPRCas9 mediated large-scale screen, with 2DG as a new tool for probing NLRP3 activation, we identified that TLR2, rather than TLR4, initiates a rapid and robust priming signal for NLRP3 inflammasome activation.

    Plasmid Preparation:

    Article Title: Genome-wide screen based on 2DG activated NLRP3 inflammasome reveals the priming signal of TLR2/4 to IKKβ but not IKKα.
    Article Snippet: NLRP3 inflammasome activation is a pivotal area of research in innate immunity, yet the precise priming and activation signal remain unclear.. In this study, we demonstrate that glycolysis inhibitor 2-Deoxy-D-glucose (2DG) triggers NLRP3-driven pyroptosis in human leukemia monocyte THP-1 cells by interfering glycosylation rather than glycolysis, which occurs independent of potassium efflux but requires the involvement of glycolysis rate-limiting enzyme PFKP.. Using a CRISPRCas9 mediated large-scale screen, with 2DG as a new tool for probing NLRP3 activation, we identified that TLR2, rather than TLR4, initiates a rapid and robust priming signal for NLRP3 inflammasome activation.

    Article Title: Genome-wide CRISPR screen reveals CLPTM1L as a lipid scramblase required for efficient glycosylphosphatidylinositol biosynthesis
    Article Snippet: .. Human GeCKOv2 CRISPR KO pooled library (Pooled Library #1000000048), pX330-U6-Chimeric_BB-CBh-hSpCas9 (Addgene plasmid #42230), and lentiCRISPR v2 (Addgene plasmid #52961) were gifts from Feng Zhang, Broad Institute of MIT and Harvard, Cambridge, MA ( , ). pX330-EGFP plasmid was generated from pX330-U6-Chimeric_BB-CBh-hSpCas9 ( ). ..

    Article Title: Genome-wide CRISPR screen reveals CLPTM1L as a lipid scramblase required for efficient glycosylphosphatidylinositol biosynthesis.
    Article Snippet: .. Human GeCKOv2 CRISPR KO pooled library (Pooled Library #1000000048), pX330-U6-Chimeric_BB-CBh-hSpCas9 (Addgene plasmid #42230), and lentiCRISPR v2 (Addgene plasmid #52961) were gifts from Feng Zhang, Broad Institute of MIT and Harvard, Cambridge, MA (15, 61). pX330EGFP plasmid was generated from pX330-U6-Chimeric_BB-CBh-hSpCas9 (62). ..

    Generated:

    Article Title: Evolutionary dynamics of heparan sulfate utilization by SARS-CoV-2.
    Article Snippet: .. CRISPR KO library-transduced HEK293T cells were generated by lentivirus-mediated transduction using the Human CRISPR KO Pooled Library (GeCKO v2; Addgene, 1000000048). ..

    Article Title: Evolutionary dynamics of heparan sulfate utilization by SARS-CoV-2
    Article Snippet: .. CRISPR KO library-transduced HEK293T cells were generated by lentivirus-mediated transduction using the Human CRISPR KO Pooled Library (GeCKO v2; Addgene, 1000000048). ..

    Article Title: Genome-wide CRISPR screen reveals CLPTM1L as a lipid scramblase required for efficient glycosylphosphatidylinositol biosynthesis
    Article Snippet: .. Human GeCKOv2 CRISPR KO pooled library (Pooled Library #1000000048), pX330-U6-Chimeric_BB-CBh-hSpCas9 (Addgene plasmid #42230), and lentiCRISPR v2 (Addgene plasmid #52961) were gifts from Feng Zhang, Broad Institute of MIT and Harvard, Cambridge, MA ( , ). pX330-EGFP plasmid was generated from pX330-U6-Chimeric_BB-CBh-hSpCas9 ( ). ..

    Article Title: Genome-wide CRISPR screen reveals CLPTM1L as a lipid scramblase required for efficient glycosylphosphatidylinositol biosynthesis.
    Article Snippet: .. Human GeCKOv2 CRISPR KO pooled library (Pooled Library #1000000048), pX330-U6-Chimeric_BB-CBh-hSpCas9 (Addgene plasmid #42230), and lentiCRISPR v2 (Addgene plasmid #52961) were gifts from Feng Zhang, Broad Institute of MIT and Harvard, Cambridge, MA (15, 61). pX330EGFP plasmid was generated from pX330-U6-Chimeric_BB-CBh-hSpCas9 (62). ..

    Transduction:

    Article Title: Evolutionary dynamics of heparan sulfate utilization by SARS-CoV-2.
    Article Snippet: .. CRISPR KO library-transduced HEK293T cells were generated by lentivirus-mediated transduction using the Human CRISPR KO Pooled Library (GeCKO v2; Addgene, 1000000048). ..

    Article Title: Evolutionary dynamics of heparan sulfate utilization by SARS-CoV-2
    Article Snippet: .. CRISPR KO library-transduced HEK293T cells were generated by lentivirus-mediated transduction using the Human CRISPR KO Pooled Library (GeCKO v2; Addgene, 1000000048). ..

    Amplification:

    Article Title: PP6 regulation of Aurora A–TPX2 limits NDC80 phosphorylation and mitotic spindle size
    Article Snippet: Transgene expression was induced by addition of 1 μg/ml doxycycline (D9891; Merck) to the culture medium for minimum of 24 h. .. Human genome targeting CRISPR KO (GeCKO) v2 lentiviral pooled libraries (A and B libraries) were purchased from Addgene and amplified according to a published protocol ( ). ..



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    ACE2-independent binding of the Omicron RBD to cell surface HS. ( A ) CRISPR KO library screening scheme to identify Omicron RBD binding molecules expressed on HEK293T cells. ( B ) Binding of CRISPR KO library-transduced HEK293T cells with (red line) or without (shaded gray) Omicron RBD-Fc, before and after sorting. ( C ) Number of sgRNA sequences identified in Omicron RBD-Fc non-binding cells after sorting. Red: GAG-synthesis-related genes; black: other expressed genes; gray: non-expressed genes in HEK293T cells. ( D ) HS biosynthetic pathway highlighting SLC35B2 and B3GAT3. PAPS, 3'-phosphoadenosine-5'-phosphosulfate; Xyl, xylose; Gal, galactose; GlcNAc, N-acetylglucosamine; GlcA, glucuronic acid; IdoA, iduronic acid. ( E ) Binding of BA.1 RBD-Fc, anti-HS Ab, or anti-CS Ab to mock (black line), or SLC35B2 or B3GAT3 KO (red line) HEK293T cells. ( F ) Binding of WT or BA.1 RBD-Fc, PILRα-Fc, anti-HS Ab, or anti-CS Ab to ACE2 KO HEK293T cells pretreated with (+) or without (–) heparinase or chondroitinase. ( G ) Binding of WT or BA.1 RBD-Fc to HEK293T cells at different heparin concentrations. RBD-Fc binding was normalized to binding in the absence of heparin. ( H ) Immunofluorescence of human nasal tissue with anti-HS Ab and 4', 6-diamidino-2-phenylindole (DAPI). Scale bar, 200 µm. ( I ) Binding of WT or BA.1 RBD-Fc, anti-ACE2 Ab, or anti-HS Ab to cell lines. Data are mean ± SEM of three to four technical replicates. Statistical analysis was performed using two-way ANOVA with Sidak’s multiple comparison tests in panel F ; * P < 0.05, ** P < 0.01, and **** P < 0.0001; ns, not significant. Data are representative of two to three independent experiments.

    Journal: mBio

    Article Title: Evolutionary dynamics of heparan sulfate utilization by SARS-CoV-2

    doi: 10.1128/mbio.01303-25

    Figure Lengend Snippet: ACE2-independent binding of the Omicron RBD to cell surface HS. ( A ) CRISPR KO library screening scheme to identify Omicron RBD binding molecules expressed on HEK293T cells. ( B ) Binding of CRISPR KO library-transduced HEK293T cells with (red line) or without (shaded gray) Omicron RBD-Fc, before and after sorting. ( C ) Number of sgRNA sequences identified in Omicron RBD-Fc non-binding cells after sorting. Red: GAG-synthesis-related genes; black: other expressed genes; gray: non-expressed genes in HEK293T cells. ( D ) HS biosynthetic pathway highlighting SLC35B2 and B3GAT3. PAPS, 3'-phosphoadenosine-5'-phosphosulfate; Xyl, xylose; Gal, galactose; GlcNAc, N-acetylglucosamine; GlcA, glucuronic acid; IdoA, iduronic acid. ( E ) Binding of BA.1 RBD-Fc, anti-HS Ab, or anti-CS Ab to mock (black line), or SLC35B2 or B3GAT3 KO (red line) HEK293T cells. ( F ) Binding of WT or BA.1 RBD-Fc, PILRα-Fc, anti-HS Ab, or anti-CS Ab to ACE2 KO HEK293T cells pretreated with (+) or without (–) heparinase or chondroitinase. ( G ) Binding of WT or BA.1 RBD-Fc to HEK293T cells at different heparin concentrations. RBD-Fc binding was normalized to binding in the absence of heparin. ( H ) Immunofluorescence of human nasal tissue with anti-HS Ab and 4', 6-diamidino-2-phenylindole (DAPI). Scale bar, 200 µm. ( I ) Binding of WT or BA.1 RBD-Fc, anti-ACE2 Ab, or anti-HS Ab to cell lines. Data are mean ± SEM of three to four technical replicates. Statistical analysis was performed using two-way ANOVA with Sidak’s multiple comparison tests in panel F ; * P < 0.05, ** P < 0.01, and **** P < 0.0001; ns, not significant. Data are representative of two to three independent experiments.

    Article Snippet: CRISPR KO library-transduced HEK293T cells were generated by lentivirus-mediated transduction using the Human CRISPR KO Pooled Library (GeCKO v2; Addgene, 1000000048).

    Techniques: Binding Assay, CRISPR, Library Screening, Immunofluorescence, Comparison

    Genome-wide CRISPR screening reveals synthetic growth defects between the catalytic subunit of PP6 and the kinetochore protein NDC80. (A) A schematic depicting the role of TPX2 in stabilization of the active pool of Aurora A at the mitotic spindle. Aurora A switches between inactive unphosphorylated (T-form) and active phosphorylated (P-form) conformations. PP6 dephosphorylates the Aurora A–TPX2 complex and promotes Aurora A inactivation. Removal of PP6 thus results in amplified Aurora A activity. (B) A cartoon outlining how the enlarged spindles in PPP6C KO cells fail to maintain the compact array of chromosomes seen in parental cells during metaphase and anaphase. Escaped chromosomes in PPP6C KO cells go on to form micronuclei and cause other nuclear shape defects. (C) Pooled genome-wide CRISPR screens were performed in parental and PPP6C KO eHAP cells. Data from two independent screens were combined and analyzed using Fisher’s method to calculate Fisher’s combined P value (FCP). Significance (−log 10 FCP) is plotted against the LFC in PPP6C KO compared with the parental cells. Significantly positively (orange) and negatively (blue) selected genes, P < 0.01 in both screens with mean LFC < 0.25 or >0.25 are highlighted on the plot.

    Journal: The Journal of Cell Biology

    Article Title: PP6 regulation of Aurora A–TPX2 limits NDC80 phosphorylation and mitotic spindle size

    doi: 10.1083/jcb.202205117

    Figure Lengend Snippet: Genome-wide CRISPR screening reveals synthetic growth defects between the catalytic subunit of PP6 and the kinetochore protein NDC80. (A) A schematic depicting the role of TPX2 in stabilization of the active pool of Aurora A at the mitotic spindle. Aurora A switches between inactive unphosphorylated (T-form) and active phosphorylated (P-form) conformations. PP6 dephosphorylates the Aurora A–TPX2 complex and promotes Aurora A inactivation. Removal of PP6 thus results in amplified Aurora A activity. (B) A cartoon outlining how the enlarged spindles in PPP6C KO cells fail to maintain the compact array of chromosomes seen in parental cells during metaphase and anaphase. Escaped chromosomes in PPP6C KO cells go on to form micronuclei and cause other nuclear shape defects. (C) Pooled genome-wide CRISPR screens were performed in parental and PPP6C KO eHAP cells. Data from two independent screens were combined and analyzed using Fisher’s method to calculate Fisher’s combined P value (FCP). Significance (−log 10 FCP) is plotted against the LFC in PPP6C KO compared with the parental cells. Significantly positively (orange) and negatively (blue) selected genes, P < 0.01 in both screens with mean LFC < 0.25 or >0.25 are highlighted on the plot.

    Article Snippet: Human genome targeting CRISPR KO (GeCKO) v2 lentiviral pooled libraries (A and B libraries) were purchased from Addgene and amplified according to a published protocol ( ).

    Techniques: Genome Wide, CRISPR, Amplification, Activity Assay

    Comparative functional genomics screening for synthetic growth defects in parental and PPP6C KO eHAP cells. (A) Workflow for genome-wide CRISPR KO screens using the GeCKO V2 libraries, with data analysis in MaGeCK comparing gene selection in PPP6C KO to parental haploid eHAP cells. (B) DNA sequence of the PPP6C genomic locus showing the sequence of candidate PPP6C KO alleles in three candidate haploid eHAP cell clones. (C) Western blot of parental eHAP and candidate PPP6C KO alleles showing loss of PPP6C protein and elevation of active Aurora A pT288. (D) Parental eHAP and PPP6C KO clone #1 stained for Aurora A pT288, tubulin, and DNA. Representative cells in metaphase are shown, with arrowheads to mark the spread of active Aurora A on the mitotic spindle. Circled areas and numbers indicate the spindle diameter in µm (ø). (E) Parental eHAP and PPP6C KO clones cells stained for NUPs and DNA. Groups of interphase cells are shown, with arrowheads to indicate micronuclei. (F) Frequency plot of median enrichment of all genes and a selected set of core essential genes (CEG) in screens 1 and 2. (G) Clonogenic survival assays for three gRNA sequences targeting NDC80 in parental and PPP6C KO eHAP cell lines. Example images of survival assays are shown. (H) Clonogenic survival assays for NDC80 gRNAs g1–g3 relative to the control gRNA in eHAP cells (mean ± SD; n = 3–5). Statistical significance was analyzed using an unpaired two-tailed t test with Welch’s correction (*, P < 0.05; **, P < 0.01). (I) Western blot validation of NDC80 depletion by the NDC80 g1–g3 gRNAs in eHAP cells. Note g2 results in reduced expression and a ladder of truncated NDC80 protein species. (J) Parental and PPP6C KO HeLa cells were treated for 48 or 72 h with siRNA for the indicated negatively selected genes identified by genome-wide screening as candidates for synthetic lethality with PPP6C KO. The proportion of morphologically abnormal nuclei is plotted in the graph. Source data are available for this figure: .

    Journal: The Journal of Cell Biology

    Article Title: PP6 regulation of Aurora A–TPX2 limits NDC80 phosphorylation and mitotic spindle size

    doi: 10.1083/jcb.202205117

    Figure Lengend Snippet: Comparative functional genomics screening for synthetic growth defects in parental and PPP6C KO eHAP cells. (A) Workflow for genome-wide CRISPR KO screens using the GeCKO V2 libraries, with data analysis in MaGeCK comparing gene selection in PPP6C KO to parental haploid eHAP cells. (B) DNA sequence of the PPP6C genomic locus showing the sequence of candidate PPP6C KO alleles in three candidate haploid eHAP cell clones. (C) Western blot of parental eHAP and candidate PPP6C KO alleles showing loss of PPP6C protein and elevation of active Aurora A pT288. (D) Parental eHAP and PPP6C KO clone #1 stained for Aurora A pT288, tubulin, and DNA. Representative cells in metaphase are shown, with arrowheads to mark the spread of active Aurora A on the mitotic spindle. Circled areas and numbers indicate the spindle diameter in µm (ø). (E) Parental eHAP and PPP6C KO clones cells stained for NUPs and DNA. Groups of interphase cells are shown, with arrowheads to indicate micronuclei. (F) Frequency plot of median enrichment of all genes and a selected set of core essential genes (CEG) in screens 1 and 2. (G) Clonogenic survival assays for three gRNA sequences targeting NDC80 in parental and PPP6C KO eHAP cell lines. Example images of survival assays are shown. (H) Clonogenic survival assays for NDC80 gRNAs g1–g3 relative to the control gRNA in eHAP cells (mean ± SD; n = 3–5). Statistical significance was analyzed using an unpaired two-tailed t test with Welch’s correction (*, P < 0.05; **, P < 0.01). (I) Western blot validation of NDC80 depletion by the NDC80 g1–g3 gRNAs in eHAP cells. Note g2 results in reduced expression and a ladder of truncated NDC80 protein species. (J) Parental and PPP6C KO HeLa cells were treated for 48 or 72 h with siRNA for the indicated negatively selected genes identified by genome-wide screening as candidates for synthetic lethality with PPP6C KO. The proportion of morphologically abnormal nuclei is plotted in the graph. Source data are available for this figure: .

    Article Snippet: Human genome targeting CRISPR KO (GeCKO) v2 lentiviral pooled libraries (A and B libraries) were purchased from Addgene and amplified according to a published protocol ( ).

    Techniques: Functional Assay, Genome Wide, CRISPR, Selection, Sequencing, Clone Assay, Western Blot, Staining, Control, Two Tailed Test, Biomarker Discovery, Expressing

    NDC80 phosphorylation and spindle checkpoint signaling are mutually exclusive. (A) HeLa MPS1-GFP CRISPR cells arrested in mitosis with either nocodazole or the proteasome inhibitor MG132 were left untreated or treated with Aurora B inhibitor (AurB-i). Cells were stained for active Aurora B pT232, phosphorylated NDC80 pS55, and the kinetochore marker CENP-C. The intensities of NDC80 pS55 signal at kinetochores and Aurora B pT232 signal are shown for the different conditions (mean ± SEM; n = 10–12; **, P < 0.01; ***, P < 0.001). (B) Parental and PPP6C KO HeLa cells arrested with STLC to create monoastral spindles with a mixture of checkpoint active and silent kinetochores states were stained for MAD1, NDC80 pS55, CENP-C, and DNA. (C and D) The intensity of NDC80 pS55 signal was measured at MAD1 positive (+ve) and negative (−ve) kinetochores (C; mean ± SD; n = 9–10), and the proportion of MAD1 or NDC80 pS55 positive kinetochores (D; mean ± SD; n = 17–34) was determined for parental and PPP6C KO HeLa cells. Statistical significance was analyzed using a Brown-Forsythe ANOVA (****, P < 0.0001).

    Journal: The Journal of Cell Biology

    Article Title: PP6 regulation of Aurora A–TPX2 limits NDC80 phosphorylation and mitotic spindle size

    doi: 10.1083/jcb.202205117

    Figure Lengend Snippet: NDC80 phosphorylation and spindle checkpoint signaling are mutually exclusive. (A) HeLa MPS1-GFP CRISPR cells arrested in mitosis with either nocodazole or the proteasome inhibitor MG132 were left untreated or treated with Aurora B inhibitor (AurB-i). Cells were stained for active Aurora B pT232, phosphorylated NDC80 pS55, and the kinetochore marker CENP-C. The intensities of NDC80 pS55 signal at kinetochores and Aurora B pT232 signal are shown for the different conditions (mean ± SEM; n = 10–12; **, P < 0.01; ***, P < 0.001). (B) Parental and PPP6C KO HeLa cells arrested with STLC to create monoastral spindles with a mixture of checkpoint active and silent kinetochores states were stained for MAD1, NDC80 pS55, CENP-C, and DNA. (C and D) The intensity of NDC80 pS55 signal was measured at MAD1 positive (+ve) and negative (−ve) kinetochores (C; mean ± SD; n = 9–10), and the proportion of MAD1 or NDC80 pS55 positive kinetochores (D; mean ± SD; n = 17–34) was determined for parental and PPP6C KO HeLa cells. Statistical significance was analyzed using a Brown-Forsythe ANOVA (****, P < 0.0001).

    Article Snippet: Human genome targeting CRISPR KO (GeCKO) v2 lentiviral pooled libraries (A and B libraries) were purchased from Addgene and amplified according to a published protocol ( ).

    Techniques: Phospho-proteomics, CRISPR, Staining, Marker