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首页> 外文期刊>RNA >SNRP-27, the C. elegans homolog of the tri-snRNP 27K protein, has a role in 5 ' splice site positioning in the spliceosome
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SNRP-27, the C. elegans homolog of the tri-snRNP 27K protein, has a role in 5 ' splice site positioning in the spliceosome

机译：SNRP-27，TRI-SNRNP 27K蛋白的C. Elegans同源物，在5英尺的剪接部位定位在抗裂纹组中的作用

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摘要

The tri-snRNP 27K protein is a component of the human U4/U6-U5 tri-snRNP and contains an N-terminal phosphorylated RS domain. In a forward genetic screen in C. elegans, we previously identified a dominant mutation, M141T, in the highlyconserved C-terminal region of this protein. The mutant allele promotes changes in cryptic 5' splice site choice. To better understand the function of this poorly characterized splicing factor, we performed high-throughput mRNA sequencing analysis on worms containing this dominant mutation. Comparison of alternative splice site usage between the mutant and wild-type strains led to the identification of 26 native genes whose splicing changes in the presence of the snrp-27 mutation. The changes in splicing are specific to alternative 5' splice sites. Analysis of new alleles suggests that snrp-27 is an essential gene for worm viability. We performed a novel directed-mutation experiment in which we used the CRISPR-cas9 system to randomly generate mutations specifically at M141 of SNRP-27. We identified eight amino acid substitutions at this position that are viable, and three that are homozygous lethal. All viable substitutions at M141 led to varying degrees of changes in alternative 5' splicing of native targets. We hypothesize a role for this SR-related factor in maintaining the position of the 5' splice site as U1snRNA trades interactions at the 5' end of the intron with U6snRNA and PRP8 as the catalytic site is assembled.
机译：三-NNRNP 27K蛋白是人U4 / U6-U5 TRI-SNRNP的组分，含有N-末端磷酸化的RS结构域。在C.埃贝朗斯的前进遗传筛查中，我们以前鉴定了在该蛋白质的高度可转化的C末端区域中的显性突变M141T。突变等位基因促进了隐秘5'剪接场地选择的变化。为了更好地理解这种表征较差的剪接因子的功能，我们对含有这种主导突变的蠕虫进行了高通量mRNA测序分析。突变体和野生型菌株之间的替代剪接部位使用的比较导致鉴定26个天然基因，其剪接SNRP-27突变存在的变化。拼接的变化是特定于替代5'拼接位点。对新等位基因的分析表明，SNRP-27是蠕虫活力的必要基因。我们进行了一种新型的突变实验，其中我们使用CRISPR-CAS9系统在SNRP-27的M141中随机产生突变。我们在该位置确定了八个氨基酸取代，以及三种是纯合的致死。 M141的所有可行性取代导致替代5'原生目标的替代5'剪接变化。我们假设该SR相关因子的作用在维持5'剪接部位的位置，因为随着催化点组装，U6SnRNA和PRP8在内含子的5'末端交易的相互作用。

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