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RECG maintains plastid and mitochondrial genome stability by suppressing extensive recombination between short dispersed repeats.

Odahara M, Masuda Y, Sato M, Wakazaki M, Harada C, Toyooka K, Sekine Y - PLoS Genet. (2015)

Bottom Line: This result suggests that mitochondrial genomic instability is responsible for the defective phenotypes of RECG KO plants.Such loci were sometimes associated with a decrease in the levels of normal mtDNA and significant decrease in the number of transcripts derived from the loci.These results suggest that RECG plays a role in the maintenance of both plastid and mitochondrial genome stability by suppressing aberrant recombination between dispersed short repeats; this role is crucial for plastid and mitochondrial functions.

View Article: PubMed Central - PubMed

Affiliation: Department of Life Science, College of Science, Rikkyo (St. Paul's) University, Toshima-ku, Tokyo, Japan.

ABSTRACT
Maintenance of plastid and mitochondrial genome stability is crucial for photosynthesis and respiration, respectively. Recently, we have reported that RECA1 maintains mitochondrial genome stability by suppressing gross rearrangements induced by aberrant recombination between short dispersed repeats in the moss Physcomitrella patens. In this study, we studied a newly identified P. patens homolog of bacterial RecG helicase, RECG, some of which is localized in both plastid and mitochondrial nucleoids. RECG partially complements recG deficiency in Escherichia coli cells. A knockout (KO) mutation of RECG caused characteristic phenotypes including growth delay and developmental and mitochondrial defects, which are similar to those of the RECA1 KO mutant. The RECG KO cells showed heterogeneity in these phenotypes. Analyses of RECG KO plants showed that mitochondrial genome was destabilized due to a recombination between 8-79 bp repeats and the pattern of the recombination partly differed from that observed in the RECA1 KO mutants. The mitochondrial DNA (mtDNA) instability was greater in severe phenotypic RECG KO cells than that in mild phenotypic ones. This result suggests that mitochondrial genomic instability is responsible for the defective phenotypes of RECG KO plants. Some of the induced recombination caused efficient genomic rearrangements in RECG KO mitochondria. Such loci were sometimes associated with a decrease in the levels of normal mtDNA and significant decrease in the number of transcripts derived from the loci. In addition, the RECG KO mutation caused remarkable plastid abnormalities and induced recombination between short repeats (12-63 bp) in the plastid DNA. These results suggest that RECG plays a role in the maintenance of both plastid and mitochondrial genome stability by suppressing aberrant recombination between dispersed short repeats; this role is crucial for plastid and mitochondrial functions.

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Complementation of the E. coli recG defect by RECG.E. coli recG-deficient cells harboring a plasmid carrying the P. patens RECG (+Pp RECG, triangle), E. coli recG (+Ec recG, circle) or empty vector (ΔrecG, square) were subjected to UV irradiation, and the surviving fraction was calculated as described in Materials and Methods. Data from three independent experiments are expressed as mean ± SD. *p<0.01 (versus ΔrecG).
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pgen.1005080.g002: Complementation of the E. coli recG defect by RECG.E. coli recG-deficient cells harboring a plasmid carrying the P. patens RECG (+Pp RECG, triangle), E. coli recG (+Ec recG, circle) or empty vector (ΔrecG, square) were subjected to UV irradiation, and the surviving fraction was calculated as described in Materials and Methods. Data from three independent experiments are expressed as mean ± SD. *p<0.01 (versus ΔrecG).

Mentions: To characterize the function of RECG, we examined whether RECG could complement the defects of an E. coli recG-deficient strain. E. coli recG-deficient strains harboring P. patens RECG lacking the signal peptide, intact E. coli recG, or no recG were subjected to UV irradiation after the induction of these genes. As reported by Ishioka et al. [27], the recG-deficient strain exhibited greater sensitivity to UV than the strain harboring the recG gene (Fig. 2), which implies that E. coli RecG participates in the recovery from UV damage. Expression of P. patens RECG conferred more than 10-fold greater resistance to UV in the recG-deficient cells, although not to the same degree as E. coli recG (Fig. 2). Therefore, RECG can partially complement the defects of E. coli recG-deficient cells.


RECG maintains plastid and mitochondrial genome stability by suppressing extensive recombination between short dispersed repeats.

Odahara M, Masuda Y, Sato M, Wakazaki M, Harada C, Toyooka K, Sekine Y - PLoS Genet. (2015)

Complementation of the E. coli recG defect by RECG.E. coli recG-deficient cells harboring a plasmid carrying the P. patens RECG (+Pp RECG, triangle), E. coli recG (+Ec recG, circle) or empty vector (ΔrecG, square) were subjected to UV irradiation, and the surviving fraction was calculated as described in Materials and Methods. Data from three independent experiments are expressed as mean ± SD. *p<0.01 (versus ΔrecG).
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4358946&req=5

pgen.1005080.g002: Complementation of the E. coli recG defect by RECG.E. coli recG-deficient cells harboring a plasmid carrying the P. patens RECG (+Pp RECG, triangle), E. coli recG (+Ec recG, circle) or empty vector (ΔrecG, square) were subjected to UV irradiation, and the surviving fraction was calculated as described in Materials and Methods. Data from three independent experiments are expressed as mean ± SD. *p<0.01 (versus ΔrecG).
Mentions: To characterize the function of RECG, we examined whether RECG could complement the defects of an E. coli recG-deficient strain. E. coli recG-deficient strains harboring P. patens RECG lacking the signal peptide, intact E. coli recG, or no recG were subjected to UV irradiation after the induction of these genes. As reported by Ishioka et al. [27], the recG-deficient strain exhibited greater sensitivity to UV than the strain harboring the recG gene (Fig. 2), which implies that E. coli RecG participates in the recovery from UV damage. Expression of P. patens RECG conferred more than 10-fold greater resistance to UV in the recG-deficient cells, although not to the same degree as E. coli recG (Fig. 2). Therefore, RECG can partially complement the defects of E. coli recG-deficient cells.

Bottom Line: This result suggests that mitochondrial genomic instability is responsible for the defective phenotypes of RECG KO plants.Such loci were sometimes associated with a decrease in the levels of normal mtDNA and significant decrease in the number of transcripts derived from the loci.These results suggest that RECG plays a role in the maintenance of both plastid and mitochondrial genome stability by suppressing aberrant recombination between dispersed short repeats; this role is crucial for plastid and mitochondrial functions.

View Article: PubMed Central - PubMed

Affiliation: Department of Life Science, College of Science, Rikkyo (St. Paul's) University, Toshima-ku, Tokyo, Japan.

ABSTRACT
Maintenance of plastid and mitochondrial genome stability is crucial for photosynthesis and respiration, respectively. Recently, we have reported that RECA1 maintains mitochondrial genome stability by suppressing gross rearrangements induced by aberrant recombination between short dispersed repeats in the moss Physcomitrella patens. In this study, we studied a newly identified P. patens homolog of bacterial RecG helicase, RECG, some of which is localized in both plastid and mitochondrial nucleoids. RECG partially complements recG deficiency in Escherichia coli cells. A knockout (KO) mutation of RECG caused characteristic phenotypes including growth delay and developmental and mitochondrial defects, which are similar to those of the RECA1 KO mutant. The RECG KO cells showed heterogeneity in these phenotypes. Analyses of RECG KO plants showed that mitochondrial genome was destabilized due to a recombination between 8-79 bp repeats and the pattern of the recombination partly differed from that observed in the RECA1 KO mutants. The mitochondrial DNA (mtDNA) instability was greater in severe phenotypic RECG KO cells than that in mild phenotypic ones. This result suggests that mitochondrial genomic instability is responsible for the defective phenotypes of RECG KO plants. Some of the induced recombination caused efficient genomic rearrangements in RECG KO mitochondria. Such loci were sometimes associated with a decrease in the levels of normal mtDNA and significant decrease in the number of transcripts derived from the loci. In addition, the RECG KO mutation caused remarkable plastid abnormalities and induced recombination between short repeats (12-63 bp) in the plastid DNA. These results suggest that RECG plays a role in the maintenance of both plastid and mitochondrial genome stability by suppressing aberrant recombination between dispersed short repeats; this role is crucial for plastid and mitochondrial functions.

Show MeSH
Related in: MedlinePlus