|Feature type||allele||Associated gene||Dmel\Met|
|Allele class||loss of function allele|
|Mutagen||X ray, 60Co gamma ray, gamma ray|
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|Nature of the Allele|
|Mutations Mapped to the Genome|
|Associated Sequence Data|
|Nature of the lesion|
Probably a chromosomal break in the transcriptional regulatory region.
|Phenotype Manifest In|
Mutant larvae are resistant to the juvenile hormone agonist pyriproxyfen compared to wild type. Mutant females show reduced fecundity: they begin ovipositing at 6.0 days after eclosion (in contrast to 3.0 days for wild-type females) and after 30 days, the total number of eggs laid by a single mutant female is only 37% that of wild type. The hatching rate of the mutant eggs is only 78%.
Mutant males treated with methoprene during larval development have normal appearing genitalia (wild-type control males show a failure of rotation of the genital disc under these conditions).
Mutant prepupae show reduced proliferation in both the outer and the inner proliferation zones of the optic lobe at an early time compared to controls. In addition, they show precocious separation of the axons of photoreceptors R7 and R8 in the medulla which is evident by 6 hours after puparium formation. The mutants show a two-hour advancement in the ingrowth of lamina neurons into the medulla compared to controls. The gross anatomy of the lamina and medulla appears normal in mutant adults and there is no mistargeting of photoreceptor axons to inappropriate layers. However, the lobula shows gross abnormalities with irregular lobes that project towards, or sometimes penetrate, the medulla neuropil. These projections severely disrupt the layering of the lobula and the lobula plate, such that neurons that normally have their dendrites confined to a single layer now project in a disorganised fashion throughout the lobula. The beginnings of these irregular projections are evident at 12 hours after puparium formation.
Rst(1)JH27 flies show good survival, with <15% mortality during pupal development. Rst(1)JH27 females show only ~20% of the level of oogenesis seen in wild-type females.
Homozygotes show increased resistance to methoprene compared to controls. Homozygous females have a reduced rate of oviposition compared to controls. 66% of mutant flies have a small number of defective ommatidia in the posterior quarter of the eye.
Under normal conditions, 1 day old mutant females show a significantly lower juvenile hormone (JH)-hydrolysing activity compared to wild-type females. Mutant and wild-type females exposed to 38oC show a significant decrease in JH-hydrolysing activity compared to control females at 25oC. 1 day old mutant females have lower levels of stress reactivity (calculated as the percent decrease in JH-hydrolysing activity at 38oC relative to normal conditions) than control females. Under normal conditions, the level of JH degradation in 5 day old mutant females is the same as in control females. After exposure to 38oC, mature mutant female show no changes in the level of JH metabolism, in contrast to control females which show a significant decrease in JH-hydrolysing activity.
Mutant females have significantly lower fertility than control flies at 25oC. At 38oC, control females show a much larger decrease in fertility compared to 25oC than mutant females.
Homozygous larvae show resistance to both the toxic and morphogenetic effects of methoprene compared to wild-type larvae. Heterozygous larvae show partial resistance to the morphogenetic effects of methoprene, but otherwise appear wild-type. Homozygous and hemizygous females show reduced oviposition; the onset of oviposition is delayed and the rate of oviposition is lower than wild-type. Homozygous females have fewer vitellogenic oocytes than wild-type females.
|NOT Enhanced by|
|NOT Enhancer of|
|Phenotype Manifest In|
|NOT Enhanced by|
Onset of metamorphosis (larval wandering stage) is delayed approximately 12 hours compared to wild type in Met gce[2.5k] double mutant larvae. Double mutant larvae and early pupae have a reduced body size compared to controls. The double mutants fail to undergo head eversion and die approximately 24 hours after pupariation. Fat body cells in the double mutants undergo precocious and enhanced programmed cell death compared to wild-type fat body cells.
Expression of gce[Scer\UAS.cBa] under the control of either Scer\GAL4[Act5C.PI], Scer\GAL4[tub.PU] or Scer\GAL4[Lsp2.PH] reduces the increased resistance to methoprene which is seen in Met animals. Met males expressing gce[Scer\UAS.cBa] under the control of Scer\GAL4[tub.PU] and treated with methoprene during larval development show abnormal genital rotation (a response similar to wild-type males raised under these conditions).
While 86% of brrbp-2/brrbp-2, Rst(1)JH27/+ flies survive to adulthood, <2% of brrbp-2/brrbp-2, Rst(1)JH27/Rst(1)JH27 flies survive this far, with most dying during the pharate adult stage. brrbp-1/brrbp-1, Rst(1)JH27/+ double mutants die at an earlier stage (prepupal/early pupal) than brrbp-1/brrbp-1 mutants. Expression of the Rst(1)JH+tSt-H.hs transgene can rescue the lethality of brrbp-2/brrbp-2, Rst(1)JH27/Rst(1)JH27 or brrbp-2/brrbp-1, Rst(1)JH27/Rst(1)JH27 flies. br1/br1, Rst(1)JH27/Rst(1)JH27 mutants are lethal in both pupal and especially pharate adult stages, but small numbers of escaper adults eclose. When these mutants express the Rst(1)JH+tSt-H.hs transgene, they survive to adulthood. Like br5 single mutants, br5, Rst(1)JH27 double mutants are lethal in prepupal/early pupal development. 54% of br5/br1, Rst(1)JH27/+ mutants survive to adulthood but br5/br1, Rst(1)JH27/Rst(1)JH27 mutants are lethal in prepupal/early pupal development. br1/br1, Rst(1)JH27/Rst(1)JH27 and brrbp-2/brrbp-2, Rst(1)JH27/Rst(1)JH27 female escapers show strong reductions in oogenesis.
|Complementation & Rescue Data|
|Fails to complement|
The lethality of Met gce[2.5k] double mutants is fully rescued by a single copy of Met[+t5.7] or by expression of gce[Scer\UAS.cBa] under the control of Scer\GAL4[arm.PS].
|Stocks ( 0 )|
|Notes on Origin|
|External Crossreferences & Linkouts|
|Synonyms & Secondary IDs ( 4 )|
(Wilson et al., 2006, Flatt and Kawecki, 2004, Wilson et al., 2002, Wilson et al., 2001, Pursley et al., 2000, Gruntenko et al., 2000, Gruntenko et al., 2000, Wilson et al., 1999, Wilson and Ashok, 1998, Wilson et al., 1998, Beno et al., 2005, Wilson et al., 2006, Baumann et al., 2010, Barry et al., 2008, Riddiford et al., 2010, Abdou et al., 2011)
|Secondary FlyBase IDs|
|References ( 18 )|