P-element insertion within the 5' untranslated region, 29bp downstream of the transcription start site.
neuroblast (with Hsp8313F3)
A Hsp83P582 background has a highly significant and reproducible effect on total phenotypic variation of scutellar and thoracic bristles. Twice as many Hsp83P582 mutant flies exhibit abnormal thoracic bristle numbers, with the severity of the thoracic bristle number defects increasing from deviations of at most two thoracic bristles to as many as four. The number of flies with aberrant scutellar bristle numbers increases 4 to 5-fold in Hsp83P582 mutants.
Hsp83P582/Hsp839J1 mutants develop until larval or early pupae. Larval brains of these mutants exhibit mitotic defects. Polyploid and other aneuploid cells make up about 30% of the mitotic figures seen. About 20% of anaphases are disorganised. The centrosome cycle is also found to be impaired in these cells. There are two classes of defect. Mitotic cells are seen containing a single microtubule organising centre (MTOC) made up of one or two unsegregated centrosomes, leading to the organisation of monopolar mitotic figures. Cells are also seen in which the centrosomes appear to fail in their assembly.
Hsp8308445/Hsp83P582 males show defects during spermatogenesis. The number and shape of spermatocytes within 16-cell cysts are mostly normal (5-10% are abnormal). Spermatids with variable number, size and shape of nuclei and nebenkern are seen. Needle-shaped crystals are present throughout developing spermatocytes and spermatids. Individualised sperm are present but they are not motile and are fragile.
Lethality occurs at embryonic or early larval stages. Mutation interacts genetically with the sev mutations; 'sev315' and sevS11.T:Hsap\MYC.
Hsp83P582/Hsp83[+] is a suppressor of arista | increased number phenotype of obk1
Hsp83P582 is rescued by Hsp83+t7.5
Hsp83P582 complements Hsp8308445 for viability and female fertility but not for male fertility.
Lethality can be rescued by Hsp83+t7.5. Hsp83+t7.5 also rescues the dominant suppression phenotype.
Excision of the P-element reverts the lethal phenotype.
Precise excision of the P-element demonstrates the insertion is responsible for the lethal phenotype.