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Thermopriming-Induced Autophagy in Shoot Apical Meristem of Arabidopsis

BACKGROUND: Since embryogenesis, plants deal with environmental changes, which might affect their growth and development. Plant autophagy has been shown to function in various stress responses, immunity, development, and senescence. Acquired thermotolerance or thermopriming is enhanced resistance to...

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Autores principales: Taheri Sedeh, Hoda, Bazgir, Eidi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: National Institute of Genetic Engineering and Biotechnology 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8926319/
https://www.ncbi.nlm.nih.gov/pubmed/35350643
http://dx.doi.org/10.30498/ijb.2021.253616.2901
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author Taheri Sedeh, Hoda
Bazgir, Eidi
author_facet Taheri Sedeh, Hoda
Bazgir, Eidi
author_sort Taheri Sedeh, Hoda
collection PubMed
description BACKGROUND: Since embryogenesis, plants deal with environmental changes, which might affect their growth and development. Plant autophagy has been shown to function in various stress responses, immunity, development, and senescence. Acquired thermotolerance or thermopriming is enhanced resistance to the elevated temperature following heat stress. OBJECTIVES: Potential contribution of autophagy mechanism after thermopriming was investigated in shoot apical meristem (SAM) of Arabidopsis thaliana. MATERIALS AND METHODS: Transcriptic expression of Autophagy related Genes (ATGs) were analyzed by qRT-PCR data in 5-day old Arabidopsis thaliana (Col0) seedlings at 4 h and 24 h after thermopriming. Autophagy induction was confirmed by confocal microscopy. RESULTS: Expression patterns of 39 ATGs and ATG-receptors were described and relevant thermopriming induced autophagy genes were identified according to their highest expression fold changes during the time after treatment. Significantly, ATG8A, ATG8B, ATG8G, ATG8H, ATI1, ATI2, NBR1, and TSPO genes were identified as the most relevant thermopriming-associated autophagy genes especially in SAM of young seedlings. This mainly implies the role of ATG8 core proteins and their receptor interactors in the regulation of autophagy in form of selective or non-selective during environmental stresses. CONCLUSIONS: Autophagy, a conserved mechanism for cell survival in plants will be activated in response to the thermopriming which is a promoted acquired resistance stimulus. Determined key genes and components of autophagy associated with thermal priming signaling pathway could be noteworthily employed to study transcriptional regulation of autophagy and integrated defense system against environmental stresses for the improvement of plant thermal tolerance and resistance to the pathogens.
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spelling pubmed-89263192022-03-28 Thermopriming-Induced Autophagy in Shoot Apical Meristem of Arabidopsis Taheri Sedeh, Hoda Bazgir, Eidi Iran J Biotechnol Research Article BACKGROUND: Since embryogenesis, plants deal with environmental changes, which might affect their growth and development. Plant autophagy has been shown to function in various stress responses, immunity, development, and senescence. Acquired thermotolerance or thermopriming is enhanced resistance to the elevated temperature following heat stress. OBJECTIVES: Potential contribution of autophagy mechanism after thermopriming was investigated in shoot apical meristem (SAM) of Arabidopsis thaliana. MATERIALS AND METHODS: Transcriptic expression of Autophagy related Genes (ATGs) were analyzed by qRT-PCR data in 5-day old Arabidopsis thaliana (Col0) seedlings at 4 h and 24 h after thermopriming. Autophagy induction was confirmed by confocal microscopy. RESULTS: Expression patterns of 39 ATGs and ATG-receptors were described and relevant thermopriming induced autophagy genes were identified according to their highest expression fold changes during the time after treatment. Significantly, ATG8A, ATG8B, ATG8G, ATG8H, ATI1, ATI2, NBR1, and TSPO genes were identified as the most relevant thermopriming-associated autophagy genes especially in SAM of young seedlings. This mainly implies the role of ATG8 core proteins and their receptor interactors in the regulation of autophagy in form of selective or non-selective during environmental stresses. CONCLUSIONS: Autophagy, a conserved mechanism for cell survival in plants will be activated in response to the thermopriming which is a promoted acquired resistance stimulus. Determined key genes and components of autophagy associated with thermal priming signaling pathway could be noteworthily employed to study transcriptional regulation of autophagy and integrated defense system against environmental stresses for the improvement of plant thermal tolerance and resistance to the pathogens. National Institute of Genetic Engineering and Biotechnology 2021-10-01 /pmc/articles/PMC8926319/ /pubmed/35350643 http://dx.doi.org/10.30498/ijb.2021.253616.2901 Text en Copyright: © 2021 The Author(s); Published by Iranian Journal of Biotechnology https://creativecommons.org/licenses/by-nc/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 Unported License, ( http://creativecommons.org/licenses/by-nc/4.0/ (https://creativecommons.org/licenses/by-nc/4.0/) ) which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Taheri Sedeh, Hoda
Bazgir, Eidi
Thermopriming-Induced Autophagy in Shoot Apical Meristem of Arabidopsis
title Thermopriming-Induced Autophagy in Shoot Apical Meristem of Arabidopsis
title_full Thermopriming-Induced Autophagy in Shoot Apical Meristem of Arabidopsis
title_fullStr Thermopriming-Induced Autophagy in Shoot Apical Meristem of Arabidopsis
title_full_unstemmed Thermopriming-Induced Autophagy in Shoot Apical Meristem of Arabidopsis
title_short Thermopriming-Induced Autophagy in Shoot Apical Meristem of Arabidopsis
title_sort thermopriming-induced autophagy in shoot apical meristem of arabidopsis
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8926319/
https://www.ncbi.nlm.nih.gov/pubmed/35350643
http://dx.doi.org/10.30498/ijb.2021.253616.2901
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