TOR and SnRK1 fine tune SPEECHLESS transcription and protein stability to optimize stomatal development in response to exogenously supplied sugar

© 2022 The Authors. New Phytologist © 2022 New Phytologist Foundation.

Bibliographische Detailangaben
Veröffentlicht in:The New phytologist. - 1979. - 234(2022), 1 vom: 05. Apr., Seite 107-121
1. Verfasser: Han, Chao (VerfasserIn)
Weitere Verfasser: Qiao, Yan, Yao, Lianmei, Hao, Wei, Liu, Yue, Shi, Wen, Fan, Min, Bai, Ming-Yi
Format: Online-Aufsatz
Sprache:English
Veröffentlicht: 2022
Zugriff auf das übergeordnete Werk:The New phytologist
Schlagworte:Journal Article Research Support, Non-U.S. Gov't Arabidopsis SPCH SnRK1 TOR stomatal development sugar availability Arabidopsis Proteins Basic Helix-Loop-Helix Transcription Factors mehr... SPEECHLESS protein, Arabidopsis Sugars TOR protein, Arabidopsis EC 2.7.1.137 Protein Serine-Threonine Kinases EC 2.7.11.1 SnRK1 protein, Arabidopsis Sirolimus W36ZG6FT64
Beschreibung
Zusammenfassung:© 2022 The Authors. New Phytologist © 2022 New Phytologist Foundation.
In Arabidopsis, the differentiation of epidermal cells into stomata is regulated by endogenous and environmental signals. Sugar is required for plant epidermal cell proliferation and differentiation. However, it is unclear how epidermal cells maintain division and differentiation to generate proper amounts of stomata in response to different sugar availability. Here, we show that two evolutionarily conserved kinase Snf1-related protein kinase 1 (SnRK1) and Target of rapamycin (TOR) play critical roles in the regulation of stomatal development under different sugar availability. When plants are grown on a medium containing 1% sucrose, sucrose-activated TOR promotes the stomatal development by inducing the expression of SPEECHLESS (SPCH), a master regulator of stomatal development. SnRK1 promotes stomatal development through phosphorylating and stabilizing SPCH. However, under the high sucrose conditions, the highly accumulated trehalose-6-phosphate (Tre6P) represses the activity of KIN10, the catalytic α-subunit of SnRK1, by reducing the interaction between KIN10 and its upstream kinase, consequently promoting SPCH degradation and inhibiting stomatal development. Our findings revealed that TOR and SnRK1 finely regulate SPCH expression and protein stability to optimize the stomatal development in response to exogenously supplied sugar
Beschreibung:Date Completed 31.03.2022
Date Revised 31.05.2022
published: Print-Electronic
Citation Status MEDLINE
ISSN:1469-8137
DOI:10.1111/nph.17984