mei41, ATR, mus103, mus104, fs(1)M37
ATM/ATR kinase, phosphatidylinositol 3-kinase - essential for the DNA damage checkpoint in larval imaginal discs and neuroblasts - required to delay mitosis in response to incomplete DNA replication in early nuclear divisions - monitors double-strand-break repair during meiotic crossing over - required for maintenance of intestinal stem cells in aging Drosophila
Gene model reviewed during 5.50
There is only one protein coding transcript and one polypeptide associated with this gene
Interacts with mus304.
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\mei-41 using the Feature Mapper tool.
GBrowse - Visual display of RNA-Seq signalsView Dmel\mei-41 in GBrowse 2
mei-41RT1 is located 0.04 map units to the right of mei-41D14 and 0.02 map units to the left of mei-41D9. mei-41RT2 is located 0.06 map units to the right of mei-41D14 and 0.03 map units to the right of mei-41D9.
Maps near 1-54.
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.
mei-41 mutants show defects in repair of double-strand breaks; they are defective in completing the later steps of homologous recombination repair, but show no defects in end-joining repair.
dsRNA made from templates generated with primers directed against this gene tested in RNAi screen for effects on Kc167 and S2R+ cell morphology.
RNAi screen using dsRNA made from templates generated with primers directed against this gene causes a phenotype when assayed in Kc167 cells: change from round to spindle-shaped, with the formation of F-actin puncta and microtubule extensions. S2R+ cells are unaffected.
The functions of mei-41 in ensuring fertility, cell cycle regulation and resistance to genotoxins are genetically separable.
The DNA damage checkpoint is inactive in the developing eye in mei-41 mutants.
Gene is involved in post-replication recombination repair, post-replication translesion synthesis repair and pre-replication DNA repair of AA lesions.
The DNA-damaging activity of 6 phenazine and aminophenazine derivatives is assayed using the wing spot test in larvae, chemicals exhibit significant mutagenicity.
The mei-41 gene has been cloned and the sequences required for its function delimited using P element mediated transformation.
mei-41 is a member of a group of proteins with a P13K-like domain. mei-41 protein is required for DNA repair and for the ability of the cell to halt the mitotic cycle at one or more points in response to DNA damage.
DNA repair test is used to evaluate the genotoxic effect of griseofulvin in somatic larval cells.
mei-41 gene product inhibits mutagenesis at early stages of oogenesis.
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-41 does not play the primary role in determining the frequency of P element excision or the variable nature of RpII2159 revertants.
mei-41 alleles confer sensitivity to mutagens as a consequence of a defect in a caffeine-sensitive post-replication repair pathway (Boyd and Setlow, 1976; Boyd, Golino, Nguyen and Green, 1976; Boyd and Shaw, 1982). This defect in DNA repair is also manifested by a high frequency of mitotic chromosome breakage and instability (Baker, Carpenter and Ripoll, 1978; Gatti, 1979). mei-411 not hypermutable to alkylation nor defective in excision repair; yet mei-41D12 displays hypermutability to alkylation and defective alkylation excision repair (Smith and Dusenberry, 1988). Allelism based on lack of complementation (Mason et al., 1989). Most alleles of mei-41 also reduce female fertility and in some cases are female-sterile as homozygotes. Females homozygous for the more fertile alleles of mei-41 exhibit reduced levels of meiotic exchange. The observed reductions in exchange are not uniform, but rather are most extreme in distal regions. Chiasma interference is also diminished (Carpenter and Sandler, 1974; Baker and Hall, 1976). These reduced levels of exchange allow for high frequencies of meiotic loss and nondisjunction (see Baker and Hall, 1976). Ultrastructural analysis of pachytene in mei-41 and mei-412 females demonstrates a reduced number of late recombination nodules which are distributed in a fashion that parallels residual exchange events (Carpenter, 1979). Over half of those nodules which are observed are morphologically abnormal and are associated with unusual regions of relatively uncondensed chromatin. Stocks in which mei-41 is carried in the male are frequently observed to carry or acquire a bb mutation on the mei-41-bearing X chromosome (Hawley and Tartof, 1983). Several alleles of mei-41 have also been shown to inhibit rDNA magnification in the male germ-line (Hawley and Tartof, 1983; Hawley et al., 1985). Moreover, mei-41 males undergoing magnification also produce a high frequency of X-Y exchanges which result from one break within the X-chromosome rDNA cluster and the other at any of a large number of sites on the Y chromosome (Hawley and Tartof, 1983).