mei-352, DmKlp3A, EG:BACR25B3.9 , fs(1)M4
Gene model reviewed during 5.50
140 (kD observed); 138 (kD predicted)
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\Klp3A using the Feature Mapper tool.
During the anaphase/telophase of female meiosis, Klp3A protein localizes to the spindle equator, in the midbody. Unlike its diffuse distribution in male meiosis, Klp3A protein is located in the spindle during metaphase, both in female meiotic cells and in syncytial blastoderm nuclei. Klp3A protein is also detected in the sperm aster and in the radial, monastral array of microtubules established between the two meiosis II spindles ("middle pole").
GBrowse - Visual display of RNA-Seq signalsView Dmel\Klp3A in GBrowse 2
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.
Experiments strongly suggest that "Klp3A" is the gene responsible for the "mei-352" mutant; Klp3A1 and Klp3A63e4 fail to complement the maternal-effect lethal phenotype of Klp3Amei-352, embryos from Klp3Amei-352/Klp3A1 transheterozygous females have a pronuclear fusion defect identical to the phenotype observed for Klp3A homozygotes and the Klp3Amei-352-bearing chromosome has a glutamic acid to lysine missense mutation in the kinesin-like motor domain of Klp3A that is not present on the parental chromosome.
RNAi screen using dsRNA made from templates generated with primers directed against this gene results in chromosome misalignment on the metaphase spindle when assayed in S2 cells. This phenotype can be observed when the screen is performed with or without Cdc27 dsRNA.
Mutations in Klp3A alter the distribution of meiotic exchanges without greatly affecting their total frequency.
Klp3A is required to establish and maintain the correct spacing between daughter nuclei during mitosis in embryos.
dsRNA made from templates generated with primers directed against this gene in S2 cells causes defects in spindle morphology and dynamics. Spindles are shorter than in wild type and spindle microtubules are highly disorganized. Additionally, the mitotic index of prometaphase and metaphase figures is higher than wild type.
dsRNA made from templates generated with primers directed against this gene tested in RNAi screen for effects on Kc167 and S2R+ cell morphology.
The major defect caused by depletion of the Klp3A protein is either in specification of the female pronucleus, or in migration of the male and female pronuclei toward each other.
Mutations have a dramatic effect on the initiation of cytokinesis in testes probably due to the disruption of microtubule interdigitation in spermatocyte central spindles. Anaphase B spindle elongation is not affected. Klp3A function is important in the establishment or stabilisation of the central spindle and this structure is the source of signals that initiate the cleavage furrow.
Klp3A function is not essential to viability but is required for fertility in both sexes. The establishment of the prominent central spindle and midbody at late anaphase/telophase requires normal Klp3A activity.
The sequence of the Klp3A protein has been compared with the sequences of a variety of kinesin family proteins.
The Klp3A+ gene product is required both during meiosis and mitosis.