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Defective autophagy through [i]epg[/i]5 mutation results in failure to reduce germ plasm and mitochondria

Authors
  • Herpin, Amaury
  • Englberger, Eva
  • Zehner, Mario
  • Wacker, Robin
  • Gessler, Manfred
  • Schartl, Manfred
Publication Date
Jan 01, 2015
Source
HAL-UPMC
Keywords
Language
English
License
Unknown
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Abstract

Autophagy is an evolutionarily conservedcatabolic process that transports cytoplasmic componentsto lysosomes for degradation. In addition to the canonicalview of strict stress-response–induced autophagy, selectivelyprogrammed autophagy was recently reported in thecontext of gonad development of flies and worms, whereautophagy seems to be necessary for clearance of germplasm components. Similar functions have not been describedin vertebrates. We used the medaka fish to studythe role of autophagy in gonad formation and gametogenesisfor the first time in a vertebrate organism for whichthegermline is specifiedby germplasm.Using a transgenicline deficient in the Ol-epg5 gene—a new critical componentof the autophagy pathway—we show that such deficiencyleads to an impaired autophagic flux, possiblyattributed to compromised maturation or processing ofthe autophagosomes. Ol-epg5 deficiency correlates withselectively impaired spermatogenesis and low allele transmissionrates of the mutant allele caused by failure of germplasm and mitochondria clearance during the process ofgerm cell specification and in the adult gonads. The mouseepg-5 homolog is similarly expressed in the maturating andadult testes, suggesting an at least partially conserved functionof this process during spermatogenesis in vertebrates.—Herpin, A., Englberger, E., Zehner, M.,Wacker, R., Gessler,M., Schartl, M. Defective autophagy through epg5 mutationresults in failure to reduce germ plasm and mitochondria.

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