In:
PLOS Genetics, Public Library of Science (PLoS), Vol. 18, No. 5 ( 2022-5-12), p. e1010202-
Kurzfassung:
Mitochondria of flowering plants have large genomes whose structure and segregation are modulated by recombination activities. The post-synaptic late steps of mitochondrial DNA (mtDNA) recombination are still poorly characterized. Here we show that RADA, a plant ortholog of bacterial RadA/Sms, is an organellar protein that drives the major branch-migration pathway of plant mitochondria. While RadA/Sms is dispensable in bacteria, RADA-deficient Arabidopsis plants are severely impacted in their development and fertility, correlating with increased mtDNA recombination across intermediate-size repeats and accumulation of recombination-generated mitochondrial subgenomes. The radA mutation is epistatic to recG1 that affects the additional branch migration activity. In contrast, the double mutation radA recA3 is lethal, underlining the importance of an alternative RECA3-dependent pathway. The physical interaction of RADA with RECA2 but not with RECA3 further indicated that RADA is required for the processing of recombination intermediates in the RECA2-depedent recombination pathway of plant mitochondria. Although RADA is dually targeted to mitochondria and chloroplasts we found little to no effects of the radA mutation on the stability of the plastidial genome. Finally, we found that the deficient maintenance of the mtDNA in radA apparently triggers a retrograde signal that activates nuclear genes repressing cell cycle progression.
Materialart:
Online-Ressource
ISSN:
1553-7404
DOI:
10.1371/journal.pgen.1010202
DOI:
10.1371/journal.pgen.1010202.g001
DOI:
10.1371/journal.pgen.1010202.g002
DOI:
10.1371/journal.pgen.1010202.g003
DOI:
10.1371/journal.pgen.1010202.g004
DOI:
10.1371/journal.pgen.1010202.g005
DOI:
10.1371/journal.pgen.1010202.g006
DOI:
10.1371/journal.pgen.1010202.g007
DOI:
10.1371/journal.pgen.1010202.g008
DOI:
10.1371/journal.pgen.1010202.g009
DOI:
10.1371/journal.pgen.1010202.g010
DOI:
10.1371/journal.pgen.1010202.s001
DOI:
10.1371/journal.pgen.1010202.s002
DOI:
10.1371/journal.pgen.1010202.s003
DOI:
10.1371/journal.pgen.1010202.s004
DOI:
10.1371/journal.pgen.1010202.s005
DOI:
10.1371/journal.pgen.1010202.s006
DOI:
10.1371/journal.pgen.1010202.s007
DOI:
10.1371/journal.pgen.1010202.s008
DOI:
10.1371/journal.pgen.1010202.s009
DOI:
10.1371/journal.pgen.1010202.s010
DOI:
10.1371/journal.pgen.1010202.s011
DOI:
10.1371/journal.pgen.1010202.r001
DOI:
10.1371/journal.pgen.1010202.r002
DOI:
10.1371/journal.pgen.1010202.r003
DOI:
10.1371/journal.pgen.1010202.r004
Sprache:
Englisch
Verlag:
Public Library of Science (PLoS)
Publikationsdatum:
2022
ZDB Id:
2186725-2
