High Light-Induced Nitric Oxide Production Induces Autophagy and Cell Death in Chlamydomonas reinhardtii
Autophagy plays a role in regulating important cellular functions in response to stress conditions. The role of nitric oxide (NO) in the regulation of autophagy in Chlamydomonas reinhardtii has been not studied. Illumination of C. reinhardtii cells under a high light (HL, 1,600 μmol m –2 s –1 ) cond...
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Published in | Frontiers in plant science Vol. 11; p. 772 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
Frontiers Media S.A
10.06.2020
|
Subjects | |
Online Access | Get full text |
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Summary: | Autophagy plays a role in regulating important cellular functions in response to stress conditions. The role of nitric oxide (NO) in the regulation of autophagy in
Chlamydomonas reinhardtii
has been not studied. Illumination of
C. reinhardtii
cells under a high light (HL, 1,600 μmol m
–2
s
–1
) condition induced a NO burst through NO synthase- and nitrate reductase-independent routes, and cell death. The abundance of CrATG8 protein, an autophagy marker of
C. reinhardtii
, increased after HL illumination along with a linear increase in the transcript abundance of autophagy-associated genes (CrVPS34, CrATG1, CrATG3, CrATG4, CrATG6, CrATG7, CrATG8, and CrATG12), which were suppressed in the presence of an NO scavenger, 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPTIO). The cells were treated with NO donors,
S
-nitroso-
N
-acetyl-penicillamine, and
S
-nitrosoglutathione, under a normal light (50 μmol m
–2
s
–1
) condition to elucidate the role of NO in autophagy activation and cell death. Treatment with 0.05 mM or 0.1 mM NO donors increased the abundance of ATG8 protein and CrATG transcripts, which were suppressed in the presence of cPTIO. Moreover, treatment with 0.05 mM NO donors did not affect cell viability, while 0.1 mM NO donors elicited a transient decrease in cell growth and death that recovered after 12 h. The transient effect could be prevented by the presence of cPTIO. However, treatment with 1 mM H
2
O
2
and 0.1 mM NO donors enhanced autophagy induction and resulted in cell death after 24 h. The interaction of H
2
O
2
and NO can be prevented by cPTIO treatment. This implies that NO is critical for the interaction of H
2
O
2
and NO that induces cell death and autophagy. Furthermore, exposure to 0.1 mM NO donors under a non-lethal HL condition (750 μmol m
–2
s
–1
) evoked autophagy and cell death. In conclusion, the present findings demonstrated that the NO-mediated autophagy pathway is activated in
C. reinhardtii
under lethal high intensity illumination and may interact with H
2
O
2
for HL-induced cell death. The relationships between autophagy and cell death are discussed. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Edited by: Dimitris Petroutsos, UMR 5168 Laboratoire de Physiologie Cellulaire Vegetale (LPCV), France This article was submitted to Plant Cell Biology, a section of the journal Frontiers in Plant Science These authors have contributed equally to this work Reviewed by: Jose L. Crespo, Consejo Superior de Investigaciones Científicas (CSIC), Spain; Thomas Roach, University of Innsbruck, Austria |
ISSN: | 1664-462X 1664-462X |
DOI: | 10.3389/fpls.2020.00772 |