Amino acid replacement: G166D.
G11617364A
G166D | Met-PA; G166D | Met-PB
G166D
Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.
Homozygotes show increased resistance to methoprene compared to controls.
18% of mutant flies have a small number of defective ommatidia in the posterior quarter of the eye.
Homozygotes fed 100μl methoprene have almost normal optic lobes, except for a very small defect in the right outer chiasm, in contrast to wild-type flies, which show widespread degeneration of the optic lobes after feeding with 100μl methoprene. In addition, homozygotes occasionally show very mild subesophageal ganglion-thoracic ganglion (SEG-TG) fusion defects when fed 100μl methoprene, in contrast to wild-type flies, which show severe SEG-TG fusion defects when fed 100μl methoprene. Homozygotes have slightly reduced numbers of muscle fibres in the retractor muscles of the rostrum of the proboscis when fed 100μl methoprene.
Homozygous, heterozygous, hemizygous and Rst(1)JHD29/Rst(1)JH1 larvae show increased resistance to Methoprene compared to wild-type. Homozygous, hemizygous and Rst(1)JHD29/Rst(1)JH1 adults derived from larvae treated with Methoprene have normal bristle patterns on sternites 6 and 7, in contrast to wild-type adults derived from larvae treated with Methoprene, which have disrupted bristle patterns on these sternites.
Flies carrying Rst(1)JH1 have a competitive disadvantage compared to wild-type flies. Pupal survival is reduced compared to wild-type.
Rst(1)JH1 mutants are 10 times more resistant than wild-type to S31183 (2-1-methyl-2-(4-phenoxyphenoxy)-ethoxy-pyridine), a juvenile hormone mimic, in a white puparial assay and about 20 times more resistant than wild-type to S31183 in a larval feeding assay.
Juvenile hormone III binding affinity and total protein accumulation in the male accessory glands is reduced.
Slightly stronger than Rst(1)JH2. Homozygotes are nearly two orders of magnitude (100x) more resistant to methoprene and juvenile hormone III than wild-type. The resistance of heterozygotes is intermediate between the homozygote and wild-type. Also resistant to methoprene induced morphogenetic abnormalities and tumours.
Semidominant mutation conferring 50-100 fold increase in resistance to juvenile hormone III or its analogue methoprene over that of wild type. Also resistant to methoprene-induced tumors and abnormalities in adult cuticle; action of Rst(1)JH autonomous in gynandromorphs. Wilson speculates that gene may affect juvenile-hormone receptor.
Met1 is a non-enhancer of abnormal chemosensory behavior | adult stage | male phenotype of Scer\GAL4Or47b.7.467, fruUAS.MB
Met1 is a non-enhancer of abnormal neurophysiology | adult stage | male phenotype of Scer\GAL4Or47b.7.467, fruUAS.MB
Met1, gce2.5k, Met27, gceMI02742 is a suppressor | partially of abnormal cell migration | parental effect | embryonic stage phenotype of HmgcrUAS.cvDa, Scer\GAL448Y
Met1 is a non-suppressor of abnormal chemosensory behavior | male | adult stage phenotype of Scer\GAL4Or47b.7.467, fruUAS.MB
Met1 is a non-suppressor of abnormal neurophysiology | male | adult stage phenotype of Scer\GAL4Or47b.7.467, fruUAS.MB
Met1/Met27, gce2.5k/gceMI02742 has partially lethal - majority die phenotype
Met1/Met27, gce2.5k/gceMI02742 has decreased fecundity phenotype
Met1/Met27, gce2.5k/gceMI02742 has abnormal cell migration | maternal effect | embryonic stage phenotype
Met1, gceMI02742 has decreased fecundity phenotype
Met1 is a non-enhancer of adult olfactory receptor neuron Or47b | male phenotype of Scer\GAL4Or47b.7.467, fruUAS.MB
Met1, gce2.5k, Met27, gceMI02742 is a suppressor | partially of primordial germ cell | parental effect | embryonic stage phenotype of HmgcrUAS.cvDa, Scer\GAL448Y
Met1 is a non-suppressor of adult olfactory receptor neuron Or47b | male phenotype of Scer\GAL4Or47b.7.467, fruUAS.MB
Met1/Met27, gce2.5k/gceMI02742 has primordial germ cell | maternal effect | embryonic stage phenotype
Analysis of gynandromorphs shows that Rst(1)JH1 acts autonomously.
The fitness component(s) responsible for the competitive disadvantage of flies carrying mutant alleles of Rst(1)JH have been analysed in Rst(1)JH1, Rst(1)JH2, Rst(1)JH3, Rst(1)JHD29 and Rst(1)JHN6 flies. Small but significant differences were found between the pooled Rst(1)JH alleles and wild-type for pupal developmental time, pupal mortality, and early adult fecundity. These differences results in a large competitive disadvantage.