Genome stability versus transcript diversity

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• 作者：Brian Magnuson^a ; ^b ; Karan Bedi^a ; Mats Ljungman^a ; ^b ; ^{ljungman@umich.edu" class="auth_mail" title="E-mail the corresponding author}
• 关键词：Pol ; (polymerase) ; BER ; (base-excision repair) ; DDR ; (DNA damage response) ; ATM ; (ataxia telangiectasia mutated) ; ATR ; (ATM-related) ; RNAPII ; (RNA polymerase II) ; CTD ; (C-terminal domain) ; AS ; (alternative splicing) ; TRAMP ; (Trf4/Air2/Mtr4p polyadenylation complex) ; NEXT ; (nuclear exosome targeting complex) ; NMD ; (nonsense-mediated decay) ; 5-FU ; (5-fluorouracil) ; UBS ; (ubiquitin-proteasome system) ; QC ; (quality control)
• 刊名：DNA Repair
• 出版年：2016
• 出版时间：August 2016
• 年：2016
• 卷：44
• 期：Complete
• 页码：81-86
• 全文大小：1025 K

文摘

Our genome is protected from the introduction of mutations by high fidelity replication and an extensive network of DNA damage response and repair mechanisms. However, the expression of our genome, via RNA and protein synthesis, allows for more diversity in translating genetic information. In addition, the splicing process has become less stringent over evolutionary time allowing for a substantial increase in the diversity of transcripts generated. The result is a diverse transcriptome and proteome that harbor selective advantages over a more tightly regulated system. Here, we describe mechanisms in place that both safeguard the genome and promote translational diversity, with emphasis on post-transcriptional RNA processing.