Nucleotide substitution: G1203T.
One of the 8 consecutive adenines between +63 to +70 region in the 5' UTR of Dic61B has been deleted, and there is a synonymous base change (G1203T) in exon 4.
A single base deletion of one of the 8 A residues in a row in the 5' UTR. Mutant also has a silent substitution in codon S198 (G to T in the third position of the codon). See GB:HQ456659 for the complete sequence of Dic61Bms21.
Homozygous Dic61Bms21 mutants develop at a similar rate to wild type. No defects are seen in the tergites or sternites.
Dic61Bms21 mutants exhibit pupal lethality when raised at 29[o]C. Approximately 18% of homozygotes and 57% of heterozygotes eclose as flies.
Dic61Bf07138 mutant testes are packed with abnormally bent sperm bundles, making the testes bulge slightly in the middle region and displacing all other cell types from their orderly arrangement. Further, their seminal vesicles are completely devoid of any sperm and appear very thin compared to the swollen vesicles seen in controls. Light squashes of mutant testes release only bundles of non-motile sperm, rather than the characteristically motile sperm seen in wild type. The individualisation complexes are well-organised, but actin cones appear disrupted soon after commencing the journey towards the caudal end of sperm tails and degrade prematurely in the middle region of the testis, before the sperm are individualised. Staining with djT:Avic\GFP-S65T shows that the progress of the actin cones is obstructed by the presence of the abnormally bent sperm tails. Aster formation and centrosomal cycling in djT:Avic\GFP-S65T testes are comparable to wild type during various stages of cell division, however mitochondrial derivatives are not properly condensed and, in contrast to wild type, the minor mitochondrial derivative is sometimes larger than the major one. The radial spokes are not uniformly organised and more than two tubules can be visualised in the central pair microtubules, apparently due to the enlargement of some of the secondary fibres. The cell boundaries are less marked in the mutant compared to wild type but the dynein arms are not severely affected, although they appear to be reduced in some of the peripheral doublets.
Homozygous males are sterile and show defects during spermatogenesis.
Homozygous males show clustering of omega speckles in cyst cells of the testes.
FlyBase curator comment: the male sterile and omega speckle phenotypes described in FBrf0199067 as being due to the Hsrω05241 mutation have subsequently been found to be due to a second site mutation on the chromosome (ms(3)2121) and are not due to an effect on Hsrω (see FBrf0205520). Compared to the 6-8 fine omega speckles in wild-type larval eye disc cells, those from ms(3)2121 homozygous larvae show 1-2 large clusters or aggregates.
FlyBase curator comment: the male sterile phenotype described in FBrf0144961 as being due to the Hsrω05241 mutation has subsequently been found to be due to a second site mutation on the chromosome (ms(3)2121) and is not due to an effect on Hsrω (see FBrf0205520). The seminal vesicles of homozygous males are very small and are completely devoid of sperm. The accessory glands and vas deferens appear normal. The organisation of the developing germ cells is abnormal in the testes; thick bundles of completely non-motile sperm appear to fill much of the internal space of the testis, which displaces the cysts of spermatocytes, resulting in their disorganised distribution in the anterior half as well as on the convex face of the testis.
Df(3L)ED201 and Df(3L)Exel6083 fail to complement the male sterile phenotype seen in Dic61Bms21.
Dic61Bc05439 fails to complement the male sterile phenotype seen in Dic61Bms21.
Dic61Bc05439 fails to complement the male sterile phenotype seen in Dic61Bms21.
Separable from: P{PZ}Hsrω05241.
The P{PZ}Hsrω05241 insertion in the promoter of Hsrω is separable from a mutation causing recessive lethality (l(3)0524105241) and also from the ms(3)2121 second site mutation.
In FBrf0144961, it was reported that the P{PZ}Hsrω05241 insertion caused male sterility and an excessive clustering of omega speckles in cyst cells in the testes. However, these phenotypes are in fact caused by the second site ms(3)2121 mutation and are not due to an effect on Hsrω.
Separable from: l(3)0524105241.