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Chlamydomonas CHT7 is involved in repressing DNA replication and mitotic genes during synchronous growth

In the green alga Chlamydomonas reinhardtii, regulation of the cell cycle in response to external cues is critical for survival in a changing environment. The loss of the nuclear COMPROMISED HYDROLYSIS OF TRIACYLGLYCEROLS 7 (CHT7) protein affects the expression of many genes especially in response t...

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Autores principales: Lin, Yang-Tsung, Takeuchi, Tomomi, Youk, Brian, Umen, James, Sears, Barbara B, Benning, Christoph
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Oxford University Press 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8895990/
https://www.ncbi.nlm.nih.gov/pubmed/35137070
http://dx.doi.org/10.1093/g3journal/jkac023
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author Lin, Yang-Tsung
Takeuchi, Tomomi
Youk, Brian
Umen, James
Sears, Barbara B
Benning, Christoph
author_facet Lin, Yang-Tsung
Takeuchi, Tomomi
Youk, Brian
Umen, James
Sears, Barbara B
Benning, Christoph
author_sort Lin, Yang-Tsung
collection PubMed
description In the green alga Chlamydomonas reinhardtii, regulation of the cell cycle in response to external cues is critical for survival in a changing environment. The loss of the nuclear COMPROMISED HYDROLYSIS OF TRIACYLGLYCEROLS 7 (CHT7) protein affects the expression of many genes especially in response to nitrogen availability. Cells lacking CHT7 exhibit abnormal cell morphology following nitrogen deprivation and fail to resume normal cell division after N resupply. To investigate the function of CHT7 in the regulation of cell cycle-related pathways, cells were synchronized, and RNA-seq analysis was performed during various stages of the cell cycle. In the cht7 mutant following nitrogen deprivation, the cells were not dividing, but a subset of cell cycle genes involved in DNA replication and mitosis were found to be derepressed, suggesting that the CHT7 protein plays a role in cell cycle regulation that is opposite to that of the mitotic cyclin-dependent kinases. Furthermore, genes for cell wall synthesis and remodeling were found to be abnormally induced in nondividing cht7 cells; this misregulation may deplete cellular resources and thus contribute to cell death following nitrogen deprivation. Lastly, 43 minimally characterized kinases were found to be highly misregulated in cht7. Further analysis suggested that some of these CHT7-regulated kinases may be related to the MAP3K and Aurora-like kinases, while others are unique. Together, these results suggest a role of CHT7 in transcriptional regulation of the cell cycle and reveal several pathways and genes whose expression appears to be subject to a CHT7-mediated regulatory network.
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spelling pubmed-88959902022-03-07 Chlamydomonas CHT7 is involved in repressing DNA replication and mitotic genes during synchronous growth Lin, Yang-Tsung Takeuchi, Tomomi Youk, Brian Umen, James Sears, Barbara B Benning, Christoph G3 (Bethesda) Investigation In the green alga Chlamydomonas reinhardtii, regulation of the cell cycle in response to external cues is critical for survival in a changing environment. The loss of the nuclear COMPROMISED HYDROLYSIS OF TRIACYLGLYCEROLS 7 (CHT7) protein affects the expression of many genes especially in response to nitrogen availability. Cells lacking CHT7 exhibit abnormal cell morphology following nitrogen deprivation and fail to resume normal cell division after N resupply. To investigate the function of CHT7 in the regulation of cell cycle-related pathways, cells were synchronized, and RNA-seq analysis was performed during various stages of the cell cycle. In the cht7 mutant following nitrogen deprivation, the cells were not dividing, but a subset of cell cycle genes involved in DNA replication and mitosis were found to be derepressed, suggesting that the CHT7 protein plays a role in cell cycle regulation that is opposite to that of the mitotic cyclin-dependent kinases. Furthermore, genes for cell wall synthesis and remodeling were found to be abnormally induced in nondividing cht7 cells; this misregulation may deplete cellular resources and thus contribute to cell death following nitrogen deprivation. Lastly, 43 minimally characterized kinases were found to be highly misregulated in cht7. Further analysis suggested that some of these CHT7-regulated kinases may be related to the MAP3K and Aurora-like kinases, while others are unique. Together, these results suggest a role of CHT7 in transcriptional regulation of the cell cycle and reveal several pathways and genes whose expression appears to be subject to a CHT7-mediated regulatory network. Oxford University Press 2022-02-07 /pmc/articles/PMC8895990/ /pubmed/35137070 http://dx.doi.org/10.1093/g3journal/jkac023 Text en © The Author(s) 2022. Published by Oxford University Press on behalf of Genetics Society of America. https://creativecommons.org/licenses/by/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Investigation
Lin, Yang-Tsung
Takeuchi, Tomomi
Youk, Brian
Umen, James
Sears, Barbara B
Benning, Christoph
Chlamydomonas CHT7 is involved in repressing DNA replication and mitotic genes during synchronous growth
title Chlamydomonas CHT7 is involved in repressing DNA replication and mitotic genes during synchronous growth
title_full Chlamydomonas CHT7 is involved in repressing DNA replication and mitotic genes during synchronous growth
title_fullStr Chlamydomonas CHT7 is involved in repressing DNA replication and mitotic genes during synchronous growth
title_full_unstemmed Chlamydomonas CHT7 is involved in repressing DNA replication and mitotic genes during synchronous growth
title_short Chlamydomonas CHT7 is involved in repressing DNA replication and mitotic genes during synchronous growth
title_sort chlamydomonas cht7 is involved in repressing dna replication and mitotic genes during synchronous growth
topic Investigation
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8895990/
https://www.ncbi.nlm.nih.gov/pubmed/35137070
http://dx.doi.org/10.1093/g3journal/jkac023
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