Nucleotide substitution: C?T.
Amino acid replacement: Q196term.
C14510821T
C?T
Q196term | HtrA2-PA; Q196term | HtrA2-PB
Q196term
HtrA2NSO/Df(3R)ED5644 mutant flies do not show any gross external defects. Females are fertile but 100% of males are sterile. In these males the seminal vesicles are empty and no motile sperm are observed.
HtrA2NSO/Df(3R)ED5644 mutant males exhibit normal mitochondrial morphology in the testes. As in wild type, the spherical "onion stage" nebenkern in the spermatids appear smooth and display no vacuolisation and the usual two mitochondrial derivatives are seen during spermatid elongation (the "leaf blade" stage). Mitochondria continue to appear normal in post-individualisation spermatids, although individual spermatids are disorganised within the cyst and the investment cones are scattered, suggesting that the movement of these structures is asynchronous.
HtrA2NSO/Df(3R)ED5644 mutants do not show any dopaminergic neuron loss in the brains of 40 day old flies at 25[o]C. Indirect flight muscles appear normal, even at 30 days, and EM analysis shows that mitochondrial integrity is as in wild type.
100% of HtrA2V110E/HtrA2NSO mutant male flies are sterile. These flies display empty seminal vesicles and no motile sperm are observed.
HtrA2NSO/Df(3R)ED5644 is a non-enhancer of spermatid phenotype of Pink15
HtrA2NSO/Df(3R)ED5644 is a non-enhancer of Nebenkern phenotype of Pink15
HtrA2NSO/Df(3R)ED5644 is a non-enhancer of mitochondrial derivative phenotype of Pink15
A HtrA2NSO/Df(3R)ED5644 mutant background does not enhance the mitochondrial morphology defects seen in Pink15 mutant spermatids.
HtrA2NSO/Df(3R)ED5644 is rescued by HtrA2βTub85D.PY
HtrA2NSO/Df(3R)ED5644 is rescued by HtrA2G363S.βTub85D
HtrA2NSO/Df(3R)ED5644 is not rescued by HtrA2S266A.βTub85D
Expression of HtrA2βTub85D.PY rescues the spermatogenesis defects seen in HtrA2NSO/Df(3R)ED5644 mutant males. Motile sperm are present in the seminal vesicles and the individualisation defects are suppressed.
Expression of HtrA2S266A.βTub85D fails to rescue the sterility seen in HtrA2NSO/Df(3R)ED5644 mutant males. In these males the seminal vesicles are empty and no motile sperm are observed.
Expression of HtrA2G363S.βTub85D rescues the sterility seen in HtrA2NSO/Df(3R)ED5644 mutant males. Motile sperm are observed in the seminal vesicles.
Complementation data shows that the semi-lethality associated with HtrA2NSO homozygotes is due to a second site mutation.