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ClNAC100 Is a NAC Transcription Factor of Chinese Fir in Response to Phosphate Starvation

Phosphate (Pi) deficiency is one of the most limiting factors for Chinese fir growth and production. Moreover, continuous cultivation of Chinese fir for multiple generations led to the reduction of soil nutrients, which hindered the yield of Chinese fir in southern China. Although NAC (NAM, ATAF, an...

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Autores principales: Zhao, Yuxuan, Huang, Shuotian, Wei, Lihui, Li, Meng, Cai, Tingting, Ma, Xiangqing, Shuai, Peng
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10341961/
https://www.ncbi.nlm.nih.gov/pubmed/37445664
http://dx.doi.org/10.3390/ijms241310486
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author Zhao, Yuxuan
Huang, Shuotian
Wei, Lihui
Li, Meng
Cai, Tingting
Ma, Xiangqing
Shuai, Peng
author_facet Zhao, Yuxuan
Huang, Shuotian
Wei, Lihui
Li, Meng
Cai, Tingting
Ma, Xiangqing
Shuai, Peng
author_sort Zhao, Yuxuan
collection PubMed
description Phosphate (Pi) deficiency is one of the most limiting factors for Chinese fir growth and production. Moreover, continuous cultivation of Chinese fir for multiple generations led to the reduction of soil nutrients, which hindered the yield of Chinese fir in southern China. Although NAC (NAM, ATAF, and CUC) transcription factors (TFs) play critical roles in plant development and abiotic stress resistance, it is still unclear how they regulate the response of Chinese fir to phosphate (Pi) starvation. Based on Pi-deficient transcriptome data of Chinses fir root, we identified a NAC transcription factor with increased expression under Pi deficiency, which was obtained by PCR and named ClNAC100. RT-qPCR confirmed that the expression of ClNAC100 in the root of Chinese fir was induced by phosphate deficiency and showed a dynamic change with time. It was positively regulated by ABA and negatively regulated by JA, and ClNAC100 was highly expressed in the roots and leaves of Chinese fir. Transcriptional activation assay confirmed that ClNAC100 was a transcriptional activator. The promoter of ClNAC100 was obtained by genome walking, which was predicted to contain a large number of stress, hormone, and growth-related cis-elements. Tobacco infection was used to verify the activity of the promoter, and the core promoter was located between −1519 bp and −589 bp. We identified 18 proteins bound to the ClNAC100 promoter and 5 ClNAC100 interacting proteins by yeast one-hybrid and yeast two-hybrid, respectively. We speculated that AHL and TIFY family transcription factors, calmodulin, and E3 ubiquitin ligase in these proteins might be important phosphorus-related proteins. These results provide a basis for the further study of the regulatory mechanism and pathways of ClNAC100 under Pi starvation.
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spelling pubmed-103419612023-07-14 ClNAC100 Is a NAC Transcription Factor of Chinese Fir in Response to Phosphate Starvation Zhao, Yuxuan Huang, Shuotian Wei, Lihui Li, Meng Cai, Tingting Ma, Xiangqing Shuai, Peng Int J Mol Sci Article Phosphate (Pi) deficiency is one of the most limiting factors for Chinese fir growth and production. Moreover, continuous cultivation of Chinese fir for multiple generations led to the reduction of soil nutrients, which hindered the yield of Chinese fir in southern China. Although NAC (NAM, ATAF, and CUC) transcription factors (TFs) play critical roles in plant development and abiotic stress resistance, it is still unclear how they regulate the response of Chinese fir to phosphate (Pi) starvation. Based on Pi-deficient transcriptome data of Chinses fir root, we identified a NAC transcription factor with increased expression under Pi deficiency, which was obtained by PCR and named ClNAC100. RT-qPCR confirmed that the expression of ClNAC100 in the root of Chinese fir was induced by phosphate deficiency and showed a dynamic change with time. It was positively regulated by ABA and negatively regulated by JA, and ClNAC100 was highly expressed in the roots and leaves of Chinese fir. Transcriptional activation assay confirmed that ClNAC100 was a transcriptional activator. The promoter of ClNAC100 was obtained by genome walking, which was predicted to contain a large number of stress, hormone, and growth-related cis-elements. Tobacco infection was used to verify the activity of the promoter, and the core promoter was located between −1519 bp and −589 bp. We identified 18 proteins bound to the ClNAC100 promoter and 5 ClNAC100 interacting proteins by yeast one-hybrid and yeast two-hybrid, respectively. We speculated that AHL and TIFY family transcription factors, calmodulin, and E3 ubiquitin ligase in these proteins might be important phosphorus-related proteins. These results provide a basis for the further study of the regulatory mechanism and pathways of ClNAC100 under Pi starvation. MDPI 2023-06-22 /pmc/articles/PMC10341961/ /pubmed/37445664 http://dx.doi.org/10.3390/ijms241310486 Text en © 2023 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Zhao, Yuxuan
Huang, Shuotian
Wei, Lihui
Li, Meng
Cai, Tingting
Ma, Xiangqing
Shuai, Peng
ClNAC100 Is a NAC Transcription Factor of Chinese Fir in Response to Phosphate Starvation
title ClNAC100 Is a NAC Transcription Factor of Chinese Fir in Response to Phosphate Starvation
title_full ClNAC100 Is a NAC Transcription Factor of Chinese Fir in Response to Phosphate Starvation
title_fullStr ClNAC100 Is a NAC Transcription Factor of Chinese Fir in Response to Phosphate Starvation
title_full_unstemmed ClNAC100 Is a NAC Transcription Factor of Chinese Fir in Response to Phosphate Starvation
title_short ClNAC100 Is a NAC Transcription Factor of Chinese Fir in Response to Phosphate Starvation
title_sort clnac100 is a nac transcription factor of chinese fir in response to phosphate starvation
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10341961/
https://www.ncbi.nlm.nih.gov/pubmed/37445664
http://dx.doi.org/10.3390/ijms241310486
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