Naslov
RecBCD- RecFOR-independent pathway of homologous recombination in Escherichia coli

Autori
Buljubašić, Maja ; Zahradka, Ksenija ; Hlevnjak, Ana ; Repar, Jelena ; Đermić, Damir ; Zahradka, Davor

Vrsta, podvrsta i kategorija rada
Sažeci sa skupova, sažetak, znanstveni

Izvornik
4th Congress of Croatian Geneticists with international participation - Book of Abstracts / Šarčević, Hrvoje ; Ugarković, Đurđica ; Vujaklija, Dušica ; Svetec, Ivan Krešimir ; Svetec Miklenić, Marina - Zagreb : Hrvatsko genetičko društvo, 2018, 25-25

ISBN
978-953-57128-1-7

Skup
4th Congress of Croatian Geneticists with international participation

Mjesto i datum
Krk, Hrvatska, 26.09.2018. - 29.09.2018

Vrsta sudjelovanja
Predavanje

Vrsta recenzije
Domaća recenzija

Ključne riječi
Recombination pathways ; RecBCD ; RecFOR ; sbcB15 mutation ; DNA repair

Sažetak
The RecA protein is a key recombinase in bacteria that catalyzes pairing and strand exchange between homologous DNA duplexes. In Escherichia coli, the RecBCD and RecFOR protein complexes mediate RecA assembly on DNA. Thus, two recombination pathways, RecBCD and RecFOR, are distinguished in E. coli. Inactivation of both recombination pathways by recB(CD) recF(OR) mutations results in severe recombination deficiency. Here we describe a novel, RecBCD- RecFOR-independent (RecBFI) recombination pathway that is active in ΔrecBCD sbcB15 sbcC(D) ΔrecF mutants. In transductional crosses, these mutants show only three-fold decrease of recombination frequency relative to the wild-type strain. At the same time, they recombine 40- to 90-fold better than their sbcB+ sbcC+ and ΔsbcB sbcC counterparts. The RecBFI pathway strongly depends on recA, recJ and recQ gene functions, moderately depends on recG and ruvABC functions, whereas inactivation of dinI, recX, recN, radA, and uvrD genes has a negligible effect. After exposure to UV and gamma- irradiation, the ΔrecBCD sbcB15 sbcC ΔrecF mutants show moderately increased DNA repair proficiency relative to their sbcB+sbcC+ and ΔsbcB sbcC counterparts. Inactivation of 3ˈ-5ˈ exonucleases ExoVII, ExoIX and ExoX does not mimic the effect of the sbcB15 mutation suggesting that protection of 3’ overhangs itself is not sufficient to enable RecBFI pathway. Rather, our results suggest that SbcB15 protein plays an active role in formation of the RecA filament.

Izvorni jezik
Engleski

Znanstvena područja
Biologija

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