mei-352, DmKlp3A, EG:BACR25B3.9 , fs(1)M4
Please see the JBrowse view of Dmel\Klp3A for information on other features
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AlphaFold produces a per-residue confidence score (pLDDT) between 0 and 100. Some regions with low pLDDT may be unstructured in isolation.
Gene model reviewed during 5.50
4.4 (unknown)
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.
The testis specificity index was calculated from modENCODE tissue expression data by Vedelek et al., 2018 to indicate the degree of testis enrichment compared to other tissues. Scores range from -2.52 (underrepresented) to 5.2 (very high testis bias).
Klp3A transcript is expressed at relatively high levels in adults of both sexes, in pupae, and embryos, but at very low levels in early larvae.
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").
During late anaphase and telophase of male meiosis, Klp3A protein localizes to the equator of the central spindle.
JBrowse - Visual display of RNA-Seq signals
View Dmel\Klp3A in JBrowsePlease 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 JBrowse 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.
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.
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.
Source for merge of: EG:BACR25B3.9 Klp3A
Source for merge of: Klp3A mei-352
Source for merge of: Klp3A BcDNA:LD21815
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.
Source for merge of Klp3A BcDNA:LD21815 was sequence comparison ( date:990717 ).