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Fig. 5 | Genome Biology

Fig. 5

From: Regulation of constitutive and alternative mRNA splicing across the human transcriptome by PRPF8 is determined by 5′ splice site strength

Fig. 5

Depletion of Complex B components that interact directly with PRPF8 recapitulate defects in mitotic progression accompanied by the altered splicing of mitotic genes. a Depletion of Complex A components does not cause defects in either the splicing of mitotic genes (top and middle panels) or in mitotic progression (bottom panel). Independent depletion of several different components of the three major spliceosome subcomplexes (A, B, and C) was verified by qRT-PCR (Additional file 5). b Depletion of several Complex B components phenocopies PRPF8, in terms of both defects in splicing of mitotic genes (top and middle panels) and, to a lesser extent, increased mitotic index (bottom panel). Depletion of the spliceosome components BRR2 and EFTUD2, which interact directly with PRPF8 to form the U5 snRNP, most strongly phenocopy PRPF8 deficiency. c Depletion of Complex C components does not cause defects in either the splicing of mitotic genes (top and middle panels), or in mitotic progression (bottom panel). SLU7 partially phenocopies PRPF8 but does not display defects in mitotic progression. For all qRT-PCR experiments in this figure, plots are relative to RNA levels in control siRNA-treated cells, assigned an arbitrary value of 1, and show the mean of triplicate readings from at least three independent depletion experiments ± standard error of the mean (SEM). For cell cycle analysis experiments, plots represent the mean from at least three independent depletion experiments ± SEM

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