RecX Facilitates Homologous Recombination by Modulating RecA Activities

Cárdenas, Paula P.; Carrasco, Begoña; Soufo, Clarisse Defeu; César, Carolina Elvira; Herr, Katharina; Kaufenstein, Miriam; Graumann, Peter L.; Alonso, Juan C.

doi:10.1371/journal.pgen.1003126

Cited by 49 publications

(95 citation statements)

References 82 publications

(162 reference statements)

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“…In B. subtilis the SOS pathway (a global response to DNA damage) were induced both by DNA damaging agents and by competence development (Love and Yasbin, 1984; Love et al, 1985; Lovett et al, 1989; Prudhomme et al, 2006). DNA uptake was not regulated by DNA damage (Redfield, 1993; Redfield et al, 1997), but in B. subtilis , the SOS system is coordinated with eDNA uptake to identify homologous regions in the genome and recombine them in order to incorporate any benefit it provides (Kidane et al, 2009, 2012; Cárdenas et al, 2012). The master regulator of competence ComK initiates the K-state (competence) differentiation by controlling the expression of a wide variety of clusters some of which relate to eDNA uptake and others to repair and recombination ( recA, dinB ; Berka et al, 2002; Hamoen et al, 2002; Ogura et al, 2002).…”

Section: Biological Functions Of Ednamentioning

confidence: 99%

Mechanisms and Regulation of Extracellular DNA Release and Its Biological Roles in Microbial Communities

2017

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The capacity to release genetic material into the extracellular medium has been reported in cultures of numerous species of bacteria, archaea, and fungi, and also in the context of multicellular microbial communities such as biofilms. Moreover, extracellular DNA (eDNA) of microbial origin is widespread in natural aquatic and terrestrial environments. Different specific mechanisms are involved in eDNA release, such as autolysis and active secretion, as well as through its association with membrane vesicles. It is noteworthy that in microorganisms, in which DNA release has been studied in detail, the production of eDNA is coordinated by the population when it reaches a certain cell density, and is induced in a subpopulation in response to the accumulation of quorum sensing signals. Interestingly, in several bacteria there is also a relationship between eDNA release and the development of natural competence (the ability to take up DNA from the environment), which is also controlled by quorum sensing. Then, what is the biological function of eDNA? A common biological role has not been proposed, since different functions have been reported depending on the microorganism. However, it seems to be important in biofilm formation, can be used as a nutrient source, and could be involved in DNA damage repair and gene transfer. This review covers several aspects of eDNA research: (i) its occurrence and distribution in natural environments, (ii) the mechanisms and regulation of its release in cultured microorganisms, and (iii) its biological roles. In addition, we propose that eDNA release could be considered a social behavior, based on its quorum sensing-dependent regulation and on the described functions of eDNA in the context of microbial communities.

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Section: Biological Functions Of Ednamentioning

confidence: 99%

Mechanisms and Regulation of Extracellular DNA Release and Its Biological Roles in Microbial Communities

2017

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“…Except for Δ recX and Δ sbcE cells, chromosomal transformation did not change more than four-fold relative to the rec + value when B. subtilis cells had a single rec − function of the α to η epistatic groups (Fernández et al, 2000) (Table 3). The absence of RecX reduced chromosomal transformation~ 50-fold (Table 3), but only 5-fold reduced in N. gonorrhoeae (Stohl and Seifert, 2001, Cardenas et al, 2012). The absence of SbcE reduced chromosomal transformation ~ 20-fold, but the absence of both SMC-like proteins, SbcE and RecN, decreased chromosomal transformation > 80-fold (Krishnamurthy et al, 2010).…”

Section: Genetic Analysis Of the Recombination Machinerymentioning

confidence: 99%

“…The absence of RecX reduced plasmid transformation by ~ 200-fold and the absence of RecO or RecU by 30- to 40-fold (Table 3) (Fernández et al, 1999, Fernández et al, 1998, Kidane et al, 2009, Cardenas et al, 2012). The above requirement is not generally conserved among competent cells, for example plasmid transformation in D. radiodurans competent cells is not affected by the absence of RecO, but is reduced (> 100-fold) in the absence of the RecO associated partner, RecR, and of another species specific single strand annealing (SSA) protein ( e.g ., DdrB) (Bouthier de la Tour et al, 2011, Satoh et al, 2012).…”

Section: Genetic Analysis Of the Recombination Machinerymentioning

confidence: 99%

“…Fourth, the modulators ( e.g ., RecF, RecX, RecU, etc .) facilitate the formation of a RecA·ssDNA filament (RecA thread) with an effectual length, both in vivo (Kidane and Graumann, 2005, Cardenas et al, 2012) or in vitro (Cox, 2007a, Galletto and Kowalczykowski, 2007). Finally, the dynamic RecA·ssDNA filaments (threads) search for a region on the resident chromosome that is homologous to incoming ssDNA.…”

Section: Functions Involved In Genetic Recombinationmentioning

confidence: 99%

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The cell pole: the site of cross talk between the DNA uptake and genetic recombination machinery

Kidane

Ayora

Sweasy

et al. 2012

Critical Reviews in Biochemistry and Molecular Biology

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Natural transformation is a programmed mechanism characterized by binding of free double-stranded (ds) DNA from the environment to the cell pole in rod-shaped bacteria. In Bacillus subtilis some competence proteins, which process the dsDNA and translocate single-stranded (ss) DNA into the cytosol, recruit a set of recombination proteins mainly to one of the cell poles. A subset of single-stranded binding proteins, working as “guardians”, protect ssDNA from degradation and limit the RecA recombinase loading. Then, the “mediators” overcome the inhibitory role of guardians, and recruit RecA onto ssDNA. A RecA·ssDNA filament searches for homology on the chromosome and, in a process that is controlled by “modulators”, catalyzes strand invasion with the generation of a displacement loop (D-loop). A D-loop resolvase or “resolver” cleaves this intermediate, limited DNA replication restores missing information and a DNA ligase seals the DNA ends. However, if any step fails, the “rescuers” will repair the broken end to rescue chromosomal transformation. If the ssDNA does not share homology with resident DNA, but it contains information for autonomous replication, guardian and mediator proteins catalyze plasmid establishment after inhibition of RecA. DNA replication and ligation reconstitute the molecule (plasmid transformation). In this review, the interacting network that leads to a cross talk between proteins of the uptake and genetic recombination machinery will be placed into prospective.

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“…Nonetheless, there are intriguing parallels between BRCA2 function in T. brucei and RecX in N. gonorrhoeae. Loss of RecX in N. gonorrhoeae impairs pilin switching (138) and, though RecX is unrelated in sequence to BRCA2, it acts in a related way, modulating RecA nucleoprotein filament formation (139,140). Hence, it seems likely that in both pathogens antigen gene recombination is controlled in ways not yet understood through the size or stability of the filaments formed by the related recombinases.…”

Section: Activation Of Intact Vsgs Involves Homologous Recombinationmentioning

confidence: 99%

DNA Recombination Strategies During Antigenic Variation in the African Trypanosome

2015

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Survival of the African trypanosome in its mammalian hosts has led to the evolution of antigenic variation, a process for evasion of adaptive immunity that has independently evolved in many other viral, bacterial and eukaryotic pathogens. The essential features of trypanosome antigenic variation have been understood for many years and comprise a dense, protective Variant Surface Glycoprotein (VSG) coat, which can be changed by recombination-based and transcription-based processes that focus on telomeric VSG gene transcription sites. However, it is only recently that the scale of this process has been truly appreciated. Genome sequencing of Trypanosoma brucei has revealed a massive archive of >1000 VSG genes, the huge majority of which are functionally impaired but are used to generate far greater numbers of VSG coats through segmental gene conversion. This chapter will discuss the implications of such VSG diversity for immune evasion by antigenic variation, and will consider how this expressed diversity can arise, drawing on a growing body of work that has begun to examine the proteins and sequences through which VSG switching is catalyzed. Most studies of trypanosome antigenic variation have focused on T. brucei , the causative agent of human sleeping sickness. Other work has begun to look at antigenic variation in animal-infective trypanosomes, and we will compare the findings that are emerging, as well as consider how antigenic variation relates to the dynamics of host–trypanosome interaction.

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RecX Facilitates Homologous Recombination by Modulating RecA Activities

Cited by 49 publications

References 82 publications

Mechanisms and Regulation of Extracellular DNA Release and Its Biological Roles in Microbial Communities

Mechanisms and Regulation of Extracellular DNA Release and Its Biological Roles in Microbial Communities

The cell pole: the site of cross talk between the DNA uptake and genetic recombination machinery

DNA Recombination Strategies During Antigenic Variation in the African Trypanosome

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