mei-41 is required for double strand break repair in the oocyte.

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.

mei-41 is essential for cell cycle arrest at high doses of X-irradiation.

Mutants of mei-41 exhibit exacerbated p53-independent cell death.

S2 cells are treated with dsRNA made from templates generated with primers directed against this gene to assess effect on proteolysis of dup and geminin genes.

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.

mei-41 has a role in delaying entry into mitosis.

The DNA damage checkpoint is inactive in the developing eye in mei-41 mutants.

mei-41 is required for precocious anaphase in Drosophila females.

mei-41 has an essential checkpoint function at the midblastula transition.

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.

The mei-9/mei-41 DNA repair test has been used to assay the DNA-damaging potency of aflatoxin B₁ and aflatoxin M₁.

Genotoxic potency of aromatic amines and polycyclic aromatic hydrocarbons can be assayed using the DNA repair assay in mei-9^a mei-41^D5 transheterozygotes.

mei-41 gene product inhibits mutagenesis at early stages of oogenesis.

The genotoxicity of a series of N-nitrosamines has been assayed using meiotic recombination deficient mei-9^a; mei-41^D5 larvae.

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-41^D12 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).