Hatching enzymes disrupt aberrant gonadal degeneration by the autophagy/apoptosis cell fate decision

Abstract Environmental stressors, gonadal degenerative diseases and tumour development can significantly alter the oocyte physiology, and species fertility and fitness. To expand the molecular understanding about oocyte degradation, we isolated several spliced variants of Japanese anchovy hatching e...

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Autores principales: Tapas Chakraborty, Sipra Mohapatra, Megumi Tobayama, Kayoko Ohta, Yong-Woon Ryu, Yukinori Kazeto, Kohei Ohta, Linyan Zhou, Yoshitaka Nagahama, Takahiro Matsubara
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Publicado: Nature Portfolio 2017
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Acceso en línea:https://doaj.org/article/18886302e23c4fdeba8cdbb7170ba575
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spelling oai:doaj.org-article:18886302e23c4fdeba8cdbb7170ba5752021-12-02T11:52:35ZHatching enzymes disrupt aberrant gonadal degeneration by the autophagy/apoptosis cell fate decision10.1038/s41598-017-03314-72045-2322https://doaj.org/article/18886302e23c4fdeba8cdbb7170ba5752017-06-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-03314-7https://doaj.org/toc/2045-2322Abstract Environmental stressors, gonadal degenerative diseases and tumour development can significantly alter the oocyte physiology, and species fertility and fitness. To expand the molecular understanding about oocyte degradation, we isolated several spliced variants of Japanese anchovy hatching enzymes (AcHEs; ovastacin homologue) 1 and 2, and analysed their potential in oocyte sustenance. Particularly, AcHE1b, an ovary-specific, steroid-regulated, methylation-dependent, stress-responsive isoform, was neofunctionalized to regulate autophagic oocyte degeneration. AcHE1a and 2 triggered apoptotic degeneration in vitellogenic and mature oocytes, respectively. Progesterone, starvation, and high temperature elevated the total degenerating oocyte population and AcHE1b transcription by hyper-demethylation. Overexpression, knockdown and intracellular zinc ion chelation study confirmed the functional significance of AcHE1b in autophagy induction, possibly to mitigate the stress effects in fish, via ion-homeostasis. Our finding chronicles the importance of AcHEs in stress-influenced apoptosis/autophagy cell fate decision and may prove significant in reproductive failure assessments, gonadal health maintenance and ovarian degenerative disease therapy.Tapas ChakrabortySipra MohapatraMegumi TobayamaKayoko OhtaYong-Woon RyuYukinori KazetoKohei OhtaLinyan ZhouYoshitaka NagahamaTakahiro MatsubaraNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-12 (2017)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Tapas Chakraborty
Sipra Mohapatra
Megumi Tobayama
Kayoko Ohta
Yong-Woon Ryu
Yukinori Kazeto
Kohei Ohta
Linyan Zhou
Yoshitaka Nagahama
Takahiro Matsubara
Hatching enzymes disrupt aberrant gonadal degeneration by the autophagy/apoptosis cell fate decision
description Abstract Environmental stressors, gonadal degenerative diseases and tumour development can significantly alter the oocyte physiology, and species fertility and fitness. To expand the molecular understanding about oocyte degradation, we isolated several spliced variants of Japanese anchovy hatching enzymes (AcHEs; ovastacin homologue) 1 and 2, and analysed their potential in oocyte sustenance. Particularly, AcHE1b, an ovary-specific, steroid-regulated, methylation-dependent, stress-responsive isoform, was neofunctionalized to regulate autophagic oocyte degeneration. AcHE1a and 2 triggered apoptotic degeneration in vitellogenic and mature oocytes, respectively. Progesterone, starvation, and high temperature elevated the total degenerating oocyte population and AcHE1b transcription by hyper-demethylation. Overexpression, knockdown and intracellular zinc ion chelation study confirmed the functional significance of AcHE1b in autophagy induction, possibly to mitigate the stress effects in fish, via ion-homeostasis. Our finding chronicles the importance of AcHEs in stress-influenced apoptosis/autophagy cell fate decision and may prove significant in reproductive failure assessments, gonadal health maintenance and ovarian degenerative disease therapy.
format article
author Tapas Chakraborty
Sipra Mohapatra
Megumi Tobayama
Kayoko Ohta
Yong-Woon Ryu
Yukinori Kazeto
Kohei Ohta
Linyan Zhou
Yoshitaka Nagahama
Takahiro Matsubara
author_facet Tapas Chakraborty
Sipra Mohapatra
Megumi Tobayama
Kayoko Ohta
Yong-Woon Ryu
Yukinori Kazeto
Kohei Ohta
Linyan Zhou
Yoshitaka Nagahama
Takahiro Matsubara
author_sort Tapas Chakraborty
title Hatching enzymes disrupt aberrant gonadal degeneration by the autophagy/apoptosis cell fate decision
title_short Hatching enzymes disrupt aberrant gonadal degeneration by the autophagy/apoptosis cell fate decision
title_full Hatching enzymes disrupt aberrant gonadal degeneration by the autophagy/apoptosis cell fate decision
title_fullStr Hatching enzymes disrupt aberrant gonadal degeneration by the autophagy/apoptosis cell fate decision
title_full_unstemmed Hatching enzymes disrupt aberrant gonadal degeneration by the autophagy/apoptosis cell fate decision
title_sort hatching enzymes disrupt aberrant gonadal degeneration by the autophagy/apoptosis cell fate decision
publisher Nature Portfolio
publishDate 2017
url https://doaj.org/article/18886302e23c4fdeba8cdbb7170ba575
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AT sipramohapatra hatchingenzymesdisruptaberrantgonadaldegenerationbytheautophagyapoptosiscellfatedecision
AT megumitobayama hatchingenzymesdisruptaberrantgonadaldegenerationbytheautophagyapoptosiscellfatedecision
AT kayokoohta hatchingenzymesdisruptaberrantgonadaldegenerationbytheautophagyapoptosiscellfatedecision
AT yongwoonryu hatchingenzymesdisruptaberrantgonadaldegenerationbytheautophagyapoptosiscellfatedecision
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