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Pharmacological Inhibition of the Spliceosome SF3b Complex by Pladienolide‐B Elicits Craniofacial Developmental Defects in Mouse and Zebrafish

• Authors : Hoshino, Yukiko; Liu, Shujie; Furutera, Toshiko ...

• Source: Birth Defects Research ; volume 116, issue 11 ; ISSN 2472-1727 2472-1727

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The SF3b complex: splicing and beyond

• Authors : Sun, Chengfu;

• Source: Cellular and Molecular Life Sciences ; volume 77, issue 18, page 3583-3595 ; ISSN 1420-682X 1420-9071

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Splicing factors of the SF3b complex PHF5A and SF3B1 regulate the DNA damage response in ALL

• Authors : Moorthy, S; Bomken, S; Ponthan, F

• Source: Klinische Pädiatrie ; 32. Jahrestagung der Kind-Philipp-Stiftung für pädiatrisch onkologische Forschung ; ISSN 1439-3824

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Structural and mechanistic insights into human splicing factor SF3b complex derived using an integrated approach guided by the cryo-EM density maps

• Authors : Rakesh, Ramachandran; Joseph, Agnel Praveen; Bhaskara, Ramachandra M.

• Source: RNA Biology ; volume 13, issue 10, page 1025-1040 ; ISSN 1547-6286 1555-8584

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CtIP-mediated Alternative mRNA Splicing Fine-tunes the DNA Damage Response

• Authors : Prados Carvajal, Rosario; Rodríguez Real, Guillermo; Gutiérrez Pozo, Gabriel ...

Subjects: CtIP; DNA damage response; MRNA splicing

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Figure 2—figure supplement 1. Characterization of SF3B1 as a CYCLOPS gene. ; (A) Growth of SF3B1gain, SF3B1control-Cal51-2 and SF3B1Loss-Cal51-2, and SF3B1K666N mutant cells (measured as change in light units; Figure 2A) after infection with shRNAs targeting LacZ or SF3B1. (B) Quantitative RT-PCR of SF3B1 expression without (black) or with (red) doxycycline-induced shSF3B1 expression using TR-shSF3B1 #5 demonstrating greater than 85% knockdown. (C) Growth of non-transformed SF3B1neutral cell lines without (black) or with (red) doxycycline-induced shSF3B1 expression using TR-shSF3B1 #5. Growth curves are measured as changes in CellTiterGlo luminescence relative to day 0 of doxycycline treatment. (D) SF3B1 immunoblot from SF3B1neutral and SF3B1loss cells expressing shLacZ (c) or shSF3B1#3 (sh3) hairpins performed in parallel to growth assays in Figure 2A. (E) Ratio of GFP-expressing cells to uninfected controls in SF3B1neutral and SF3B1loss breast and hematopoietic cell lines expressing shLacZ-GFP (black) or shSF3B1#4-GFP (red). (F) Heatmap of False Discovery Rate q-values indicating the significance of associations between copy numbers of SF3b complex members (rows) and sensitivity of those cells to suppression of SF3b complex members by shRNA (columns). (G) PHF5A immunoblot three days after infection with shLacZ or shPHF5A targeting hairpins from HCC1954 cells profiled in panel Figure 2—figure supplement 1G. (H) Growth of breast cancer cell lines expressing shLacZ (black) or shPHF5A (red), measured as changes in CellTiterGlo luminescence relative the day of infection. For all panels, error bars represent ± SD from at least three technical replicates.

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Rewards of divergence in sequences, 3-D structures and dynamics of yeast and human spliceosome SF3b complexes

• Authors : Arangasamy Yazhini; Sankaran Sandhya; Narayanaswamy Srinivasan

Subjects: SF3b complex; Spliceosome; Cryo-EM structure

• Source: Current Research in Structural Biology, Vol 3, Iss , Pp 133-145 (2021)

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Figure 4—figure supplement 1. SF3B1 copy-loss selectively reduces the abundance of the SF3b complex. ; (A) Sedimentation of mass standards in 10–30% glycerol gradients. (B) Elution profiles of mass standards in gel filtration chromatography columns. (C) Quantification of SF3B1 immunoblots from serial dilutions of glycerol gradient fractions in Figure 4G. SF3B1 abundance normalized by actin loading controls and calculated by densitometry using ImageJ (see Appendix Methods). SF3B1neutral and SF3B1loss cells (n = 2 each) quantified from western blot images performed in triplicate. Dots represent mean and error bars are ± SD. (D) Immunoblot of indicated gel filtration fractions. GAPDH and SNRPB2 represent markers for complexes

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Figure 4. SF3B1 copy-loss selectively reduces the abundance of the SF3b complex. ; (A) Diagram of U2 snRNP assembly. (B–C) Glycerol gradient fractionation of native whole-cell lysates probed by western blot in breast cancer cell lines and (D–E) isogenic cells generated by CRISPR. (F) Quantification of SF3B1 immunoblots from glycerol gradient fractions 3–8, relative to fraction 3 (n = 3 for each group, see Appendix Methods). (G) Serial dilution of pooled glycerol gradient fractions probed for SF3B1 by immunoblot. (H) (left) SF3B1 Native PAGE immunoblot of pooled glycerol gradient fractions. (right) denaturing silver stain of total protein from the same pooled fractions as loading control. (I) Quantitative RT-PCR for U2 snRNA expression in three SF3B1neutral and three SF3B1loss breast cancer cell lines. (J) Native agarose gel of U2 snRNP complexes visualized with radiolabeled 2’ O-methyl oligonucleotides complementary to the U2 snRNA. Nuclear extracts were generated from SF3B1control-Cal51 and SF3B1Loss-Cal51 cells. HeLa cell nuclear extracts (NE) ± ATP were used as controls. Representative image from triplicate experiments. (K) Densitometric quantification of 17S U2 snRNP bands in (J) presented as fold change relative to SF3B1control-Cal51 cells. Data are from three replicate experiments. (L) Model for changes to U2 snRNP assembly associated with SF3B1 copy-loss. For all panels, *p

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CRISPR directed evolution of the spliceosome for resistance to splicing inhibitors

• Authors : Butt, Haroon; Eid, Ayman; Momin, Afaque ...

Subjects: Directed evolution; Genome engineering; Spliceosome

• Source: ISSN: 1465-6906.

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