Ramírez-Santos Jesús, García-Mata Verónica, Poggio Sebastian, Camarena Laura, Gómez-Eichelmann M Carmen
Departamento de Biología Molecular y Biotecnología, Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, P.O. Box 70-228, 04510 Mexico, D.F., Mexico.
Arch Microbiol. 2009 Feb;191(2):185-90. doi: 10.1007/s00203-008-0441-z. Epub 2008 Nov 19.
In RecBCD(+) cells, a mutated single-strand DNA 3'-5' exonuclease ExoI (SbcB15) induced an increase in stationary-phase mutation. In sbcB15 cells, as in wild-type cells, these mutations partially required RecA, RecB, RecF, and expression of the LexA regulon. The absence of nuclease SbcCD in sbcB15 cells decreased stationary-phase mutation and induced an increase in the number of cell filaments. The absence of ExoI (Deltaxon) in wild-type or sbcC cells did not change significantly the stationary-phase mutation. Differences between the sbcB15 and DeltaxonA cells suggest a correlation between level of SOS induction and the generation of stationary-phase mutations.
在RecBCD(+)细胞中,一种突变的单链DNA 3'-5'核酸外切酶ExoI(SbcB15)导致稳定期突变增加。在sbcB15细胞中,与野生型细胞一样,这些突变部分需要RecA、RecB、RecF以及LexA调控子的表达。sbcB15细胞中核酸酶SbcCD的缺失降低了稳定期突变,并导致细胞丝状化数量增加。野生型或sbcC细胞中ExoI(Deltaxon)的缺失并未显著改变稳定期突变。sbcB15和DeltaxonA细胞之间的差异表明SOS诱导水平与稳定期突变的产生之间存在相关性。