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2016 ; 5
(ä): ä Nephropedia Template TP
gab.com Text
Twit Text FOAVip
Twit Text #
English Wikipedia
Elimination of paternal mitochondria in mouse embryos occurs through autophagic
degradation dependent on PARKIN and MUL1
#MMPMID27852436
Rojansky R
; Cha MY
; Chan DC
Elife
2016[Nov]; 5
(ä): ä PMID27852436
show ga
A defining feature of mitochondria is their maternal mode of inheritance.
However, little is understood about the cellular mechanism through which paternal
mitochondria, delivered from sperm, are eliminated from early mammalian embryos.
Autophagy has been implicated in nematodes, but whether this mechanism is
conserved in mammals has been disputed. Here, we show that cultured mouse
fibroblasts and pre-implantation embryos use a common pathway for elimination of
mitochondria. Both situations utilize mitophagy, in which mitochondria are
sequestered by autophagosomes and delivered to lysosomes for degradation. The E3
ubiquitin ligases PARKIN and MUL1 play redundant roles in elimination of paternal
mitochondria. The process is associated with depolarization of paternal
mitochondria and additionally requires the mitochondrial outer membrane protein
FIS1, the autophagy adaptor P62, and PINK1 kinase. Our results indicate that
strict maternal transmission of mitochondria relies on mitophagy and uncover a
collaboration between MUL1 and PARKIN in this process.