RESUMO
DNA mismatch repair (MMR) is a highly conserved pathway in evolution responsible for maintaining genomic stability. MMR is initiated when MutS proteins recognize and repair single base-base mismatches and small loops of unpaired nucleotides as well as certain types of DNA damage. Arabidopsis thaliana and other plants contain MutS protein homologs (MSH) found in other eukaryotic organisms and a unique MSH7 polypeptide. In this study, we first evaluated transient expression profiles of ten-days old pAtMSH7:GUS transgenic seedlings at different recovery times after an acute treatment for 48 hs with100 mM NaCl. GUS histochemical staining indicated that MSH7 expression is repressed by salt exposure but recovers progressively. Then, ten-days old mutants harboring two independent msh7 alleles were exposed for 48 hs with100 mM NaCl and different traits were measured over recovery time. Salt treated msh7 seedlings were defective in G2/M arrest. As a result, msh7 seedlings showed a reduced salt inhibitory effect as evidenced by a decreased reduction of rosette and leaf areas, stomatal density, total leaf number, silique length and seed number per silique. These findings suggest that disruption of MSH7 activity could be a promising approach for plant adaptive responses to salinity stress.
Assuntos
Proteínas de Arabidopsis , Arabidopsis , Apoptose , Arabidopsis/genética , Arabidopsis/metabolismo , Proteínas de Arabidopsis/genética , Proteínas de Arabidopsis/metabolismo , Pontos de Checagem do Ciclo Celular , Reparo de Erro de Pareamento de DNA , Pontos de Checagem da Fase G2 do Ciclo Celular , Estresse SalinoRESUMO
DNA mismatch repair (MMR) is a highly conserved biological pathway that improves the fidelity of DNA replication and recombination. MMR is initiated when MutS proteins recognize mismatches and small loops of unpaired nucleotides. Arabidopsis thaliana and other plants encode MutS protein homologs (MSH) conserved among other eukaryotic organisms, but also encode an extra MSH polypeptide (MSH7). In order to better understand the role of MSH7 in vivo, a full set of phenotypic parameters that covered the development of the plant from seed imbibition to flowering and seed maturation was analyzed in A. thaliana harboring two different msh7 alleles. Plants deficient in MSH7 show statistically significant faster germination rates, longer primary roots during the juvenile vegetative phase, and higher cauline leaf and axillary and lateral inflorescence numbers compared with wild type. We also quantified number, length and area of siliques and seed number per silique. Disruption of MSH7 resulted in a higher number of smaller siliques than wild type. There were no differences in seed number per silique between genotypes. These findings suggest that mutant plant growth appears to be caused by an impaired cell cycle checkpoint that allows cell division without adequate DNA repair. This increase in proliferation activity demonstrates a functional and temporal link between DNA repair and cell cycle regulation.