, ▁V D AC 3 ▁plays ▁an ▁important ▁role ▁in ▁the ▁mit och ond rial ▁cell ▁death ▁path way ▁trans du ction ▁here by ▁reg ulating ▁apo pt otic ▁signal ing ▁and ▁cell ▁death . ▁ ▁As ▁V D AC 3 ▁is ▁a ▁reg ulator ▁of ▁s perm ▁mot ility , ▁male ▁m ice ▁missing ▁V D AC 3 ▁result ▁in ▁infer til ity . ▁Mut ations ▁in ▁V D AC 3 ▁are ▁also ▁associated ▁with ▁Park inson ’ s ▁disease , ▁as ▁V D AC 3 ▁has ▁been ▁observed ▁to ▁target ▁Park in ▁to ▁defect ive ▁mit och ond ria ▁to ▁eliminate ▁them ▁by ▁mit oph agy . ▁Fail ure ▁to ▁eliminate ▁these ▁mit och ond ria ▁result ▁in ▁the ▁accum ulation ▁of ▁re active ▁o xygen ▁species , ▁the ▁commonly ▁attributed ▁cause ▁of ▁Park inson ’ s ▁disease . ▁In ▁addition , ▁it ▁has ▁been ▁found ▁that ▁V D AC 3 - null ▁m ice ▁were ▁born ▁at ▁the ▁expected ▁m end elian ▁ratio . ▁Mut ant ▁females ▁were ▁fert ile , ▁but ▁males ▁were ▁not ▁due ▁to ▁marked ly ▁reduced ▁s perm ▁mot ility . ▁The ▁majority ▁of ▁e pid id ym al ▁ax on emes ▁showed ▁struct ural ▁defect s , ▁most ▁commonly ▁loss ▁of ▁a ▁single ▁micro t ub ule ▁double t ▁at ▁a ▁conser ved ▁position ▁within ▁the ▁ax on eme . ▁In ▁test icular ▁s perm , ▁the ▁defect ▁was ▁only ▁rarely ▁observed , ▁suggesting ▁that ▁inst ability ▁of ▁a ▁normally ▁formed ▁ax on eme ▁occurred