High impact information on okr

• Strand pairing by Rad54 and Rad51 is enhanced by chromatin [1].
• okra and spindle-B encode components of the RAD52 DNA repair pathway and affect meiosis and patterning in Drosophila oogenesis [2].
• In functional tests of their role in DNA repair, we find that okr behaves like its yeast homolog in that it is required in both mitotic and meiotic cells [2].
• A Drosophila melanogaster strain deficient in the RAD54 homolog DmRAD54 is characterized by increased X-ray and methyl methanesulfonate (MMS) sensitivity [3].
• However, whereas X-ray-induced loss-of-heterozygosity (LOH) events were completely absent in DmRAD54(-/-) flies, treatment with cross-linking agents or MMS resulted in only a slight reduction in LOH events in comparison with those in wild-type flies [3].

Biological context of okr

• Of these, mutants deficient in DNA repair, mei-41 and okra, show progressive degeneration of imaginal discs and die as pupae, while other genotypes survive to adulthood after irradiation [4].
• The genes okra and spindle-B act during meiosis in Drosophila to repair double-stranded DNA breaks (DSBs) associated with meiotic recombination [5].
• To determine the function of DmRAD54, a null mutant was isolated by random mutagenesis [6].
• PCR analysis indicated that the undamaged homologous chromosome may compensate for the potential loss of the broken chromosome in rad54 mutant females after excision [7].

Regulatory relationships of okr

• The Drosophila melanogaster DNA Ligase IV gene plays a crucial role in the repair of radiation-induced DNA double-strand breaks and acts synergistically with Rad54 [8].

Other interactions of okr

• Mutations in the genes okra, mus309, and mei41 did not affect eccDNA under normal conditions or following mutagen treatment, implying that eccDNA formation is different from known pathways of DNA repair [9].
• To determine the relative contribution of NHEJ and homologous recombination (HR) in Drosophila, Lig4; Rad54 double-mutant flies were generated [8].
• Here we show that enc mutants also exhibit abnormalities in karyosome morphology, similar to other ventralizing mutants such as okra and spindle B [10].

References