
대장균에서 RecBCD 발현은 Hfq 단백질에 의한 전사 후 조절을 통해 최적의 수준으로 유지된다.


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All living organisms have developed strategies to respond to chromosomal damage and preserve genome integrity. One such response is the repair of DNA double-strand breaks (DSBs), one of the most toxic forms of DNA lesions. In Escherichia coli , DSBs are repaired via RecBCD-dependent homologous recombination. RecBCD is essential for accurate chromosome maintenance, but its over-expression can lead to reduced DNA repair ability. This apparent paradox suggests that RecBCD copy numbers may need to be tightly controlled within an optimal range. Using single-molecule fluorescence mi-croscopy, we have established that RecB is present in very low abundance at mRNA and protein levels. RecB transcription shows high fluctuations, yet cell-to-cell protein variability remains remarkably low. Here, we show that the post-transcriptional regulator Hfq binds to recB mRNA and down-regulates RecB protein translation in vivo . Furthermore, specific disruption of the Hfq-binding site leads to more efficient translation of recB mRNAs. In addition, we observe a less effective reduction of RecB protein fluctuations in the absence of Hfq. This fine-tuning Hfq-mediated mechanism might have the underlying physiological function of maintaining RecB protein levels within an optimal range.

### Competing Interest Statement

The authors have declared no competing interest.

An Hfq-dependent post-transcriptional mechanism fine tunes RecB expression in Escherichia coli

대장균의-recbcd-발현-미세조정은-최적의-dna-수리를-위해-필요한-전사-후-조절


대장균의 RecBCD 발현 미세조정은 최적의 DNA 수리를 위해 필요한 전사 후 조절
