The RNA repair proteins RtcAB regulate transcription activator RtcR via its CRISPR-associated Rossmann fold domain.
The RNA repair proteins RtcAB regulate transcription activator RtcR via its CRISPR-associated Rossmann fold domain.
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DOI:
10.1016/j.isci.2022.105425
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发表时间:
2022-11-18
期刊:
影响因子:
5.8
通讯作者:
Engl, Christoph
中科院分区:
文献类型:
--
作者:
Kotta-Loizou, Ioly;Giuliano, Maria Grazia;Jovanovic, Milija;Schaefer, Jorrit;Ye, Fuzhou;Zhang, Nan;Irakleidi, Danai Athina;Liu, Xiaojiao;Zhang, Xiaodong;Buck, Martin;Engl, Christoph
CRISPR-associated Rossmann fold (CARF) domain signaling underpins modulation of CRISPR-Cas nucleases; however, the RtcR CARF domain controls expression of two conserved RNA repair enzymes, cyclase RtcA and ligase RtcB. Here, we demonstrate that RtcAB are required for RtcR-dependent transcription activation and directly bind to RtcR CARF. RtcAB catalytic activity is not required for complex formation with CARF, but is essential yet not sufficient for RtcRAB-dependent transcription activation, implying the need for an additional RNA repair-dependent activating signal. This signal differs from oligoadenylates, a known ligand of CARF domains, and instead appears to originate from the translation apparatus: RtcB repairs a tmRNA that rescues stalled ribosomes and increases translation elongation speed. Taken together, our data provide evidence for an expanded range for CARF domain signaling, including the first evidence of its control via in trans protein-protein interactions, and a feed-forward mechanism to regulate RNA repair required for a functioning translation apparatus. RtcR physically interacts with RtcB and RtcA via its regulatory CARF domain RtcR-RtcBA interactions positively control rtcBA expression The transfer-messenger RNA ssrA is a target of rtc inducing stress RtcB impacts the speed of translation elongation Molecular biology; Molecular mechanism of gene regulation; Cell biology
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影响因子:
5.2
作者:
Abo T;Chadani Y
通讯作者:
Chadani Y
DOI:
10.1093/bioinformatics/btu638
发表时间:
2015-01-15
期刊:
Bioinformatics (Oxford, England)
影响因子:
--
作者:
Anders S;Pyl PT;Huber W
通讯作者:
Huber W
影响因子:
5.6
作者:
Joly N;Burrows PC;Engl C;Jovanovic G;Buck M
通讯作者:
Buck M
影响因子:
56.9
作者:
Jinek, Martin;Chylinski, Krzysztof;Charpentier, Emmanuelle
通讯作者:
Charpentier, Emmanuelle
影响因子:
16.8
作者:
Boël G;Smith PC;Ning W;Englander MT;Chen B;Hashem Y;Testa AJ;Fischer JJ;Wieden HJ;Frank J;Gonzalez RL Jr;Hunt JF
通讯作者:
Hunt JF