Insertion WG1288 of Bellen, Genes Dev 3:1288 , within 10bp of site of insertion of P in RpS6air8 in 5' untranslated region of RpS6. Impossible to determine precise insertion site as a small duplication accompanied insertion of P{lArB} element.
RpS6WG1288/RpS6WG1288 embryonic macrophages do not show any changes in the phagocytic index (apoptotic cells clearance) compared to wild-type.
The prothoracic gland is 35% smaller than normal in heterozygous third instar larvae.
Heterozygotes show a delay in eclosion of up to 18 hours compared to wild type. This delay is reduced by the addition of 20-hydroxyecdysone.
Hemizygous males are developmentally delayed at all stages. Lethality generally occurs during extended third instar period when melanotic tumours arise.
Melanotic tumour phenotype similar to that of RpS6air8.
RpS6WG1288/RpS6[+] is a suppressor of visible phenotype of CycEJP
RpS6WG1288/RpS6[+] is a non-suppressor of decreased occurrence of cell division | larval stage phenotype of CycEJP
RpS6WG1288/RpS6WG1288 is a suppressor of embryonic/larval plasmatocyte | embryonic stage phenotype of pallko
RpS6WG1288/RpS6[+] is a suppressor of eye phenotype of CycEJP
RpS6WG1288/RpS6[+] is a non-suppressor of embryonic/larval plasmatocyte | embryonic stage phenotype of pallko
RpS6WG1288/RpS6[+] is a non-suppressor of eye disc phenotype of CycEJP
The defects in phagocytic apoptotic cells clearance displayed by homozygous pallko mutant embryos can be rescued by combination with RpS6WG1288 in homozygous, but not heterozygous state.
RpS6WG1288/+ restores eye size and reduces eye roughness in CycEJP homozygous adults. The number of mitotic cells in the second mitotic wave in the CycEJP eye disc is not increased by RpS6WG1288/+.
The addition of 20-hydroxyecdysone prevents the suppression of the CycEJP eye phenotype by RpS6WG1288/+.
RpS6WG1288 is rescued by Scer\GAL4P0206/RpS6UAS.cLa
Expression of RpS6Scer\UAS.cLa under the control of Scer\GAL4P0206 suppresses the developmental delay seen in RpS6WG1288/+ flies.
Lethality is reverted by excision of the P{lArB} element, demonstrating the element to be responsible for the mutant phenotype.