Homozygous clu^d08713 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

clu^ΔW/clu^d08713 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 clu^ΔW/clu^d08713 adults are not apoptotic (assessed by TUNEL assay).

Mitochondria are mislocalized and highly clustered in clu^d08713/clu^d08713 germ cells in the ovary, clu^d08713/clu^d08713 females are sterile (never lay eggs), and both males and females have locomotor (climbing ability) defects. Mitochondria disperse normally in clu^d08713/+ germ cells in the ovary.

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.

clu^d08713 has short lived phenotype, suppressible | partially by Scer\GAL4^da.PU

clu^d08713 has abnormal developmental rate phenotype, suppressible | partially by Scer\GAL4^da.PU

clu^d08713 has female sterile phenotype, suppressible by Scer\GAL4^da.PU/Hsap\CLUH^UASp.cSa

clu^d08713 has abnormal locomotor behavior | adult stage phenotype, suppressible by Scer\GAL4^da.PU/Hsap\CLUH^UASp.cSa

clu^d08713 has mitochondrion phenotype, suppressible by Scer\GAL4^da.PU/Hsap\CLUH^UASp.cSa

clu^d08713 has ovary phenotype, suppressible by Scer\GAL4^da.PU/Hsap\CLUH^UASp.cSa

Pink1^B9, clu^d08713/clu[+] has ovary phenotype

Pink1^B9, clu^d08713/clu[+] has mitochondrion phenotype