short lived (with Df(2R)Jp4)
Homozygous clud08713 show significant delay in the onset of pupariation compared to controls and the eclosing adults are extremely short lived and die before day 5 of adult life
cluΔW/clud08713 transheterozygous mutant third instar larvae display mitochondrial morphology defects - clustered, rounded mitochondria - in larval muscles and these larvae also display significant locomotion deficit (reduced crawling speed).
Indirect flight muscles in 4-day-old cluΔW/clud08713 adults are not apoptotic (assessed by TUNEL assay).
Mutant third instar larval brains have a normal overall structure and the number of neuroblasts in each anterior ventral brain hemisphere in homozygotes is the same as in heterozygous controls.
Mitochondria are mislocalised and clumped throughout the cell cycle in mutant neuroblasts. This mislocalisation does not appear to affect the percent total mitochondria volume per cell volume in the mutant neuroblasts.
Mutant larvae pupate at normal rates, but with a three day delay. Only 40% of the pupae eclose, with the remainder dying as pharate adults. Animals that do survive to adulthood die very quickly after eclosion.
Adult viability of homozygotes is 4%. Homozygous adults are small, uncoordinated, sterile and live for only 3-7 days after eclosion. The adults move slowly, do not fly and frequently hold their wings up or down. The adults contain persistent larval fat body cells, failing to turn them over within the first two days of adult life.
Flight muscles of homozygous adults have abnormal, swollen mitochondria which show extensive vacuolisation of the inner membrane and loss of cristae. Mitochondria in the ovaries of homozygous females also show similar, but less severe defects, including reduced cristae and swelling.
Mitochondria show abnormal localisation in mutant ovaries. In the germline stem cells, the mitochondria nearly all occupy the anterior region of the cell (in wild-type ovaries, mitochondria are enriched anteriorly but are also found throughout the cytoplasm). Mitochondria in the mutant ovaries also cluster in stage 5 nurse cells and cluster at the ends of the fusome in later cysts, in contrast to wild type. The distribution of microtubules in the ovary is not affected in the mutant females.
clud08713 has short lived phenotype, suppressible | partially by Scer\GAL4da.PU
clud08713 has abnormal developmental rate phenotype, suppressible | partially by Scer\GAL4da.PU
clud08713 has female sterile phenotype, suppressible by Scer\GAL4da.PU/Hsap\CLUHUASp.cSa
clud08713 has abnormal locomotor behavior | adult stage phenotype, suppressible by Scer\GAL4da.PU/Hsap\CLUHUASp.cSa
clud08713 has mitochondrion phenotype, suppressible by Scer\GAL4da.PU/Hsap\CLUHUASp.cSa
clud08713 has ovary phenotype, suppressible by Scer\GAL4da.PU/Hsap\CLUHUASp.cSa
Pink1B9, clud08713/clu[+] has mitochondrion phenotype
Expression of Hsap\CLUHScer\UAS.P\T.cSa under the control of Scer\GAL4da.PU partially rescues both the pupariation delay and the extremely short lifespan of clud08713 homozygotes: majority of flies survive past post-eclosion day 5 and display longevity comparable to wild-type.
Expression of Hsap\CLUHScer\UAS.P\T.cSa driven by Scer\GAL4da.PU rescues the mislocalization and clustering of mitochondria seen in germ cells in clud08713/clud08713 ovaries, as well as female sterility (egg-laying ability) and locomotor defects (climbing ability) in clud08713/clud08713 flies.
clud08713 is rescued by cluUASp.cSa
cluΔW/clud08713 is rescued by cluUAS.Tag:MYC/Scer\GAL4Mef2.PR
clud08713 is rescued by Scer\GAL4da.PU/cluUASp.cSa
clud08713 is not rescued by cluΔβGF.UASp
clud08713 is not rescued by cluΔDUF.UASp
clud08713 is not rescued by cluΔClu.UASp
clud08713 is not rescued by cluΔM.UASp
clud08713 is not rescued by cluΔTPR.UASp
clud08713 is not rescued by cluΔcterm.UASp
Expression of cluScer\UAS.P\T.cSa under the control of Scer\GAL4da.PU rescues the extremely short lifespan of clud08713 homozygote adults: practically all flies survive past post-eclosion day 5 and display longevity comparable to wild-type.
Expression of any of the following: cluΔβGF.Scer\UAS.P\T, cluΔDUF.Scer\UAS.P\T, cluΔClu.Scer\UAS.P\T, cluΔM.Scer\UAS.P\T, cluΔTPR.Scer\UAS.P\T or cluΔcterm.Scer\UAS.P\T under the control of Scer\GAL4da.PU fails to rescue both the delay in the onset of pupariation and the extremely short lifespan of clud08713 homozygote adults: all flies fail to survive past post-eclosion day 5.
The abnormal mitochondrial morphology - clustered, rounded mitochondria - observed in muscles 6 and 7 of cluΔW/clud08713 mutant larvae can be rescued to wild-type appearance by Scer\GAL4Mef2.PR-driven expression of cluUAS.Tag:MYC (which on its own also induces defects in mitochondrial morphology).
Expression of cluScer\UAS.P\T.cSa driven by Scer\GAL4da.PU rescues the mislocalization and clustering of mitochondria seen in germ cells in clud08713/clud08713 ovaries, as well as female sterility (egg-laying ability) and locomotor defects (climbing ability) in clud08713/clud08713 flies.