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Long-distance transport of sucrose in source leaves promotes sink root growth by the EIN3-SUC2 module
In most plants, sucrose, a major storage sugar, is transported into sink organs to support their growth. This key physiological process is dependent on the function of sucrose transporters. Sucrose export from source tissues is predominantly controlled through the activity of SUCROSE TRANSPORTER 2 (...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Public Library of Science
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9529141/ https://www.ncbi.nlm.nih.gov/pubmed/36129930 http://dx.doi.org/10.1371/journal.pgen.1010424 |
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author | Tong, Chen Li, Cong Cao, Xiao-Ying Sun, Xu-Dong Bao, Qin-Xin Mu, Xin-Rong Liu, Chang-Yue Loake, Gary J. Chen, Hu-hui Meng, Lai-Sheng |
author_facet | Tong, Chen Li, Cong Cao, Xiao-Ying Sun, Xu-Dong Bao, Qin-Xin Mu, Xin-Rong Liu, Chang-Yue Loake, Gary J. Chen, Hu-hui Meng, Lai-Sheng |
author_sort | Tong, Chen |
collection | PubMed |
description | In most plants, sucrose, a major storage sugar, is transported into sink organs to support their growth. This key physiological process is dependent on the function of sucrose transporters. Sucrose export from source tissues is predominantly controlled through the activity of SUCROSE TRANSPORTER 2 (SUC2), required for the loading of sucrose into the phloem of Arabidopsis plants. However, how SUC2 activity is controlled to support root growth remains unclear. Glucose is perceived via the function of HEXOKINASE 1 (HXK1), the only known nuclear glucose sensor. HXK1 negatively regulates the stability of ETHYLENE-INSENSITIVE3 (EIN3), a key ethylene/glucose interaction component. Here we show that HXK1 functions upstream of EIN3 in the regulation of root sink growth mediated by glucose signaling. Furthermore, the transcription factor EIN3 directly inhibits SUC2 activity by binding to the SUC2 promoter, regulating glucose signaling linked to root sink growth. We demonstrate that these molecular components form a HXK1-EIN3-SUC2 module integral to the control of root sink growth. Also, we demonstrate that with increasing age, the HXK1-EIN3-SUC2 module promotes sucrose phloem loading in source tissues thereby elevating sucrose levels in sink roots. As a result, glucose signaling mediated-sink root growth is facilitated. Our findings thus establish a direct molecular link between the HXK1-EIN3-SUC2 module, the source-to sink transport of sucrose and root growth. |
format | Online Article Text |
id | pubmed-9529141 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Public Library of Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-95291412022-10-04 Long-distance transport of sucrose in source leaves promotes sink root growth by the EIN3-SUC2 module Tong, Chen Li, Cong Cao, Xiao-Ying Sun, Xu-Dong Bao, Qin-Xin Mu, Xin-Rong Liu, Chang-Yue Loake, Gary J. Chen, Hu-hui Meng, Lai-Sheng PLoS Genet Research Article In most plants, sucrose, a major storage sugar, is transported into sink organs to support their growth. This key physiological process is dependent on the function of sucrose transporters. Sucrose export from source tissues is predominantly controlled through the activity of SUCROSE TRANSPORTER 2 (SUC2), required for the loading of sucrose into the phloem of Arabidopsis plants. However, how SUC2 activity is controlled to support root growth remains unclear. Glucose is perceived via the function of HEXOKINASE 1 (HXK1), the only known nuclear glucose sensor. HXK1 negatively regulates the stability of ETHYLENE-INSENSITIVE3 (EIN3), a key ethylene/glucose interaction component. Here we show that HXK1 functions upstream of EIN3 in the regulation of root sink growth mediated by glucose signaling. Furthermore, the transcription factor EIN3 directly inhibits SUC2 activity by binding to the SUC2 promoter, regulating glucose signaling linked to root sink growth. We demonstrate that these molecular components form a HXK1-EIN3-SUC2 module integral to the control of root sink growth. Also, we demonstrate that with increasing age, the HXK1-EIN3-SUC2 module promotes sucrose phloem loading in source tissues thereby elevating sucrose levels in sink roots. As a result, glucose signaling mediated-sink root growth is facilitated. Our findings thus establish a direct molecular link between the HXK1-EIN3-SUC2 module, the source-to sink transport of sucrose and root growth. Public Library of Science 2022-09-21 /pmc/articles/PMC9529141/ /pubmed/36129930 http://dx.doi.org/10.1371/journal.pgen.1010424 Text en © 2022 Tong et al 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 use, distribution, and reproduction in any medium, provided the original author and source are credited. |
spellingShingle | Research Article Tong, Chen Li, Cong Cao, Xiao-Ying Sun, Xu-Dong Bao, Qin-Xin Mu, Xin-Rong Liu, Chang-Yue Loake, Gary J. Chen, Hu-hui Meng, Lai-Sheng Long-distance transport of sucrose in source leaves promotes sink root growth by the EIN3-SUC2 module |
title | Long-distance transport of sucrose in source leaves promotes sink root growth by the EIN3-SUC2 module |
title_full | Long-distance transport of sucrose in source leaves promotes sink root growth by the EIN3-SUC2 module |
title_fullStr | Long-distance transport of sucrose in source leaves promotes sink root growth by the EIN3-SUC2 module |
title_full_unstemmed | Long-distance transport of sucrose in source leaves promotes sink root growth by the EIN3-SUC2 module |
title_short | Long-distance transport of sucrose in source leaves promotes sink root growth by the EIN3-SUC2 module |
title_sort | long-distance transport of sucrose in source leaves promotes sink root growth by the ein3-suc2 module |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9529141/ https://www.ncbi.nlm.nih.gov/pubmed/36129930 http://dx.doi.org/10.1371/journal.pgen.1010424 |
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