kl3, Lms3
Please see the JBrowse view of Dmel\kl-3 for information on other features
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Gene model reviewed during 6.01
Gene model reviewed during 6.02
There is only one protein coding transcript and one polypeptide associated with this gene
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\kl-3 using the Feature Mapper tool.
GBrowse - Visual display of RNA-Seq signals
View Dmel\kl-3 in GBrowse 2Y-
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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 merge of: kl-3 CG17629
Source for merge of: kl-3 CG40992 CG40936
Annotations CG40992, CG40936 and CG17629 merged as CG45785 in release 6.02 of the genome annotation. This gene is no longer fragmented in the release 6 genome assembly.
Source for merge of kl-3 CG17629 was sequence comparison ( date:001108 ).
Williamson (1972) reported 23 non-complementing and nine complementing alleles induced by EMS.
Sequence of transcript(s) changed in r6 genomic release relative to r5 release.
New annotation (CG40992) in release 5.2 of the genome annotation.
New annotation (CG40936) in release 5.2 of the genome annotation.
Transiently named CG40443 in release 3 of the genome annotation.
It is not yet known if "ms(Y)104b" is the same as kl-3.
Males mutant for kl-3 fail to assemble the outer dynein arms associated with the peripheral nine microtubule doublets of the sperm-tail axoneme (Hardy, Tokuyasu, and Lindsley, 1981). Such males also fail to produce a kl-3-specific 300-325 kilodalton sperm polypeptide presumed to be a component of the outer dynein arms (Goldstein, Hardy and Lindsley, 198). Such mutants display an exceedingly low level of fertility at 25oC but not at 18oC immediately upon eclosion, but not thereafter (Kennison, 1983). Deficiencies for kl-3 are completely sterile, and in addition to the above mutant phenotype, they fail to elaborate the loops (ribbon-like structure) observed in the primary spermatocyte nuclei of normal males by light microscopy and the reticular material ordinarily observed by electron microscopy in spermatocyte nuclei (Hardy et al., 1981). The kl-3 loops are visible in living spermatocytes and in fixed cells stained with the protein-specific dye CBB; these loops are also demonstrated by the polyclonal antibody Sph-155 but do not react with monoclonal antibody S5 (Bonaccorsi et al., 1988).