Low-frequency RNA-Seq exon junction(s) not annotated.
Gene model reviewed during 5.52
Heterodimer (By similarity). Interacts with hdm.
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\mei-9 using the Feature Mapper tool.
GBrowse - Visual display of RNA-Seq signalsView Dmel\mei-9 in GBrowse 2
Please Note FlyBase no longer curates genomic clone accessions so this list may not be complete
Please Note This section lists cDNAs and ESTs that fall within the genomic extent of the gene model, which may include cDNAs and ESTs of genes within introns, or of overlapping genes. Please see GBrowse for alignment of the cDNAs and ESTs to the gene model.
For each fully sequenced cDNA the DGRC maintains various forms of the cDNA (e.g tagged or untagged) in several different host vectors for subsequent cloning and expression in Drosophila and Drosophila cell lines.
Source for identity of: mei-9 CG3697
The underlying meiotic function for mei-9 appears to be in crossover formation rather than mismatch repair, as in the absence of mei-9 activity, postmeiotic segregation associated with noncrossovers occurs at the expense of crossover products.
Extracts from Drosophila embryos and adults generated from mei-9 mutants have specific defects in DNA mismatch repair.
Gene is involved in pre-replication DNA repair of UV and AA lesions.
Sex-linked recessive lethal (SLRL) test is used to demonstrate inactivation of the nucleotide excision repair (NER) system has a major impact on mutational response of germ cells to mutagens.
A positional mapping strategy combined with a differential expression assay is used to clone mei-9, mei-9 is homologous to yeast repair gene RAD1, and the mei-9 transcript is absent in mei-9A3 mutants.
The DNA-damaging activity of 6 phenazine and aminophenazine derivatives is assayed using the wing spot test in larvae, chemicals exhibit significant mutagenicity.
DNA repair test is used to evaluate the genotoxic effect of griseofulvin in somatic larval cells.
The effects of repair deficiency are studied by comparing the frequency of somatic mutation and mitotic recombination in repair proficient female progeny with that in excision repair defective male progeny. Nine chemical mutagens with various modes of action are tested in this way.
An unusually high level of P-M hybrid dysgenesis is characteristic of hybrid offspring originating from Harwich P strain crosses. The phenotype is greatly exacerbated when males are deficient either in excision repair (mei-9 mutation) or in post-replication repair (mei-41 mutation). These findings demonstrate that both DNA repair pathways are essential for the repair of lesions induced by P-element transposition.
mei-9 does not play the primary role in determining the frequency of P element excision or the variable nature of RpII2159 revertants.
mei-9 alleles confer sensitivity to mutagens as a consequence of a defect in excision repair (Boyd et al., 1976; Nguyen and Boyd, 1977). This defect in DNA repair is also manifested by a high frequency of mitotic chromosome breakage and instability (Baker et al., 1978; Gatti, 1979). For example, larval neuroblasts of mei-9/Y males display a high frequency of spontaneous chromosome breaks in both the eu- and heterochromatin (Gatti, 1979). Females homozygous for mei-9 show greatly reduced levels of meiotic exchange. However, the residual exchanges are distributed as in wild-type and chiasma interference is maintained. mei-9 is thus considered to be defective in the exchange process itself, rather than in the establishment of the preconditions for exchange (Carpenter and Sandler, 1974). mei-9a and mei-9b have also been assayed with respect to their effects on gene conversion at the rosy locus (Carpenter, 1982). Although neither allele reduces the frequency of gene conversion events, both produce post-meiotic segregation events (i.e., mosaic progeny) at high frequency. Thus, the recombinational phenotype of mei-9 involves two components, namely a decrease in the frequency of heteroduplex repair and a decrease in the frequency of reciprocal exchange. At the ultrastructural level, both synaptonemal complex morphology and the number and distribution of recombination nodules are normal in mei-9 females (Carpenter, 1979); but see Boyd et al. (1976). As a consequence of the decreased frequency of reciprocal exchange, mei-9 females display greatly elevated frequencies of meiotic nondisjunction and chromosome loss (Baker and Carpenter, 1972). Meiotic chromosome behavior in males is not affected. Nor is there any effect of mei-9 on spontaneous recombination in males (Lutken and Baker, 1979). Neither hypermutable to alkylation nor deficient in excision repair (Smith and Dusenberry, 1988).