Imprecise excision of the P{EP}EP2269 insertion, resulting in a 1.8kb deletion that removes the mir-8 gene.
mir-8Δ2/Df(2R)BSC382 males show a significant increase in median lifespan compared to controls.
3-5 day old mir-8Δ2/Df(2R)mir-8Δ3 adults show reduced climbing ability in a negative geotaxis assay.
mir-8Δ2/Df(2R)mir-8Δ3 adults show significant defects in the hemolymph-brain barrier (as determined using a dye injection assay).
Homozygous larvae show a significant reduction in evoked excitatory junctional potential (EJP) amplitude at the neuromuscular junction compared to controls. Amplitude of the spontaneous miniature EJP (mEJP) is normal, but mEJP frequency and quantal content are reduced.
The neuroepithelium of mir-8Δ2 L3 larvae is 143% overgrown compared to wild type. In the subsequent stage, ectopic and precocious neuroblasts are scattered throughout this enlarged neuroepithelium.
Wing size is reduced by 10% compared to controls in mir-8Δ2/Df(2R)mir-8Δ3 adults, and the wings have extra veins.
Mutant male and female adults are significantly smaller in size and mass than wild-type controls. Mutant adults have a reduced wing size which is caused by reduced wing cell number with no significant change in cell size.
Mutant larvae have a significantly smaller body volume than wild-type larvae at 100 hours after egg laying. The onset of pupariation occurs at the normal time, however, there is a slight delay in adult emergence in the mutant animals.
Cells of homozygous clones in the fat body are smaller than the adjacent wild-type twin-spot cells. When homozygous clones are induced in the fat body at the embryonic or newly hatched larval stage, few or no homozygous cells are seen next to the wild-type twin spots, suggesting a failure of proliferation and survival of the mutant cells during larval development. Homozygous clones in the wing or eye disc have little growth defects.
Homozygous mir-8Δ2 mutants show a malformed adult third leg phenotype. No defects are observed in early leg disc patterning and morphogenesis. Neuromuscular junction defects are seen in third instar larvae.
A mir-8Δ2/+ background enhances the malformed third leg phenotype seen when mir-8sponge.Scer\UAS.T:Avic\GFP-EGFP is expressed under the control of Scer\GAL4αTub84B.PL.
A mir-8Δ2/+ background enhances the third instar larval neuromuscular junction phenotypes seen when mir-8sponge.Scer\UAS.T:Avic\GFP-EGFP is expressed under the control of Scer\GAL4αTub84B.PL.
No detectable neuromuscular junction phenotypes are seen when mir-8sponge.Scer\UAS.T:Avic\GFP-EGFP is expressed under the control of Scer\GAL4elav.PLu in a mir-8Δ2/+ background.
Flies expressing mir-8sponge.Scer\UAS.T:Avic\GFP-EGFP in a mir-8Δ2 background under the control of the leg specific driver Scer\GAL4Dll.PU appear indistinguishable from controls.
Mutants show no defects in targeting of the DL1 glomerulus in the antennal lobe.
mir-8Δ1/mir-8Δ2 and mir-8Δ2/Df(2R)mir-8Δ3 animals show reduced survival during pupal and early adult stages, either failing to emerge from the pupal case or dying within the first 24 hours of eclosion.
mir-8Δ1/mir-8Δ2 and mir-8Δ2/Df(2R)mir-8Δ3 adult escapers often have wing defects (the wings are not properly unfolded) or leg defects.
mir-8Δ2/Df(2R)mir-8Δ3 third instar larvae show increased levels of apoptosis in the brain compared to controls.
3 day old mir-8Δ2/Df(2R)mir-8Δ3 adults perform less well in a climbing assay than controls, and the severity of the defect is increased in 9 day old flies.
mir-8Δ2/Df(2R)mir-8Δ3 has visible phenotype, suppressible | partially by Ser[+]/SerRX106
mir-8Δ2/Df(2R)mir-8Δ3 has abnormal size phenotype, suppressible by Ser[+]/SerRX106
mir-8Δ2 has decreased body size phenotype, suppressible by Scer\GAL4Cg.PA/ushVDRC.cUa
mir-8Δ2 has decreased body size phenotype, suppressible by ush[+]/ush1513
mir-8Δ2 has decreased body size phenotype, suppressible by Hsap\MIR200CUAS.cHa/Scer\GAL4Cg.PA/Hsap\MIR141UAS.cHa
mir-8Δ2 has decreased body size phenotype, suppressible by Hsap\MIR200CUAS.cHa/Scer\GAL4ppl.PP/Hsap\MIR141UAS.cHa
mir-8Δ2 has abnormal neuroanatomy phenotype, suppressible | partially by ena[+]/ena210
mir-8Δ2 has abnormal neuroanatomy phenotype, suppressible by Lmon\actAFP4mito.UAS.EGFP/Scer\GAL4how-24B
mir-8Δ2/Df(2R)mir-8Δ3 has abnormal locomotor behavior | adult stage phenotype, suppressible by Gug35/Gug[+]
mir-8Δ2/Df(2R)mir-8Δ3 has partially lethal phenotype, suppressible | partially by Gug35/Gug[+]
mir-8Δ2/Df(2R)mir-8Δ3 has partially lethal phenotype, suppressible | partially by BacA\p35UAS.cHa
miPEP-8alt/miPEP-8[+], mir-8Δ2 has visible | adult stage phenotype
miPEP-8alt/miPEP-8[+], mir-8Δ2 has decreased size | adult stage phenotype
mir-8Δ2/Df(2R)mir-8Δ3 has wing phenotype, suppressible by Ser[+]/SerRX106
mir-8Δ2 has embryonic/larval neuromuscular junction | third instar larval stage phenotype, suppressible | partially by ena[+]/ena210
mir-8Δ2 has NMJ bouton | larval stage phenotype, suppressible | partially by ena[+]/ena210
mir-8Δ2 has embryonic/larval neuromuscular junction | third instar larval stage phenotype, suppressible by Lmon\actAFP4mito.UAS.EGFP/Scer\GAL4how-24B
mir-8Δ2 has NMJ bouton | larval stage phenotype, suppressible by Lmon\actAFP4mito.UAS.EGFP/Scer\GAL4how-24B
mir-8Δ2/Df(2R)mir-8Δ3 has leg phenotype, suppressible | partially by Gug35/Gug[+]
miPEP-8alt/miPEP-8[+], mir-8Δ2 has wing phenotype
miPEP-8alt/+, mir-8Δ2/+ individuals show a small wing.
SerRX106/+ fully rescues the defects in wing size and partially suppresses the extra wing vein phenotype caused by mir-8Δ2/Df(2R)mir-8Δ3.
Expression of ushVDRC.cUa under the control of Scer\GAL4Cg.PA significantly rescues the reduced weight of mir-8Δ2 adults.
ush1513/+ significantly rescues the reduced weight of mir-8Δ2 adults.
The survival defect of mir-8Δ2/Df(2R)mir-8Δ3 animals is partially suppressed by Gug35/+. The proportion of surviving adults that have leg defects is also reduced in the double mutants and the leg malformations are less severe than those seen in mir-8Δ2/Df(2R)mir-8Δ3 single mutants.
The impairment in climbing ability that is seen in 3 and 9 day old mir-8Δ2/Df(2R)mir-8Δ3 adults is less severe if the flies also carry Gug35/+.
Expression of P{UAS-mir-200-c} (which encodes Hsap\MIR200CScer\UAS.cHa and Hsap\MIR141Scer\UAS.cHa) under the control of either Scer\GAL4Cg.PA or Scer\GAL4ppl.PP rescues the reduced weight of mir-8Δ2 adults to near that of wild type.
Expression of Zzzz\actAFP4mito.Scer\UAS.T:Avic\GFP-EGFP under the control of Scer\GAL4how-24B rescues the neuromuscular junction phenotypes seen in mir-8Δ2 larvae.
The survival defect of mir-8Δ2/Df(2R)mir-8Δ3 animals is partially suppressed by low-level expression of BacA\p35Scer\UAS.cHa (in the absence of a Scer\GAL4 driver).
mir-8Δ2 is rescued by mir-8UAS.cHa/Scer\GAL4Cg.PA
mir-8Δ2 is rescued by mir-8UAS.cHa/Scer\GAL4ppl.PP
mir-8Δ2 is not rescued by mir-8UAS.cHa/Scer\GAL4elav.PU
Expression of mir-8Scer\UAS.cHa under the control of either Scer\GAL4Cg.PA or Scer\GAL4ppl.PP rescues the reduced weight of mir-8Δ2 adults to near that of wild type.
Expression of mir-8Scer\UAS.cHa under the control of Scer\GAL4elav.PU does not rescue the reduced weight of mir-8Δ2 adults.