Glucose-driven TOR-FIE-PRC2 signalling controls plant development.
Glucose-driven TOR-FIE-PRC2 signalling controls plant development.
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DOI:
10.1038/s41586-022-05171-5
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发表时间:
2022-09
期刊:
影响因子:
64.8
通讯作者:
Sheen, Jen
中科院分区:
文献类型:
--
作者:
Ye, Ruiqiang;Wang, Meiyue;Du, Hao;Chhajed, Shweta;Koh, Jin;Liu, Kun-hsiang;Shin, Jinwoo;Wu, Yue;Shi, Lin;Xu, Lin;Chen, Sixue;Zhang, Yijing;Sheen, Jen
Nutrients and energy have emerged as central modulators of developmental programs in plants and animals. The evolutionarily conserved target-of-rapamycin (TOR) kinase is a master integrator of nutrient and energy signalling that controls growth. Despite its important regulatory roles in translation, proliferation, metabolism, and autophagy, little is known about how TOR shapes developmental transitions and differentiation. Here we show that glucose-activated TOR kinase controls genome-wide histone H3 trimethylation at K27 (H3K27me3) that regulates cell fates and development. We identify FERTILIZATION-INDEPENDENT-ENDOSPERM (FIE), an indispensable component of Polycomb repressive complex 2 (PRC2) catalysing H3K27me3, as a surprising TOR target. Direct TOR phosphorylation promotes dynamic cytoplasm-to-nucleus translocation of FIE. The targeted FIE phosphorylation mutation abrogates global H3K27me3 landscape, reprograms transcriptome, and disrupts organogenesis in plants. Moreover, glucose-TOR-FIE-PRC2 signalling modulates vernalization-induced floral transition. We propose that this newly defined signalling axis serves as a nutritional checkpoint leading to epigenetic silencing of key transcription factor genes that specify stem-cell destiny in shoot and root meristems and control leaf, flower and silique patterning, branching, and vegetative-to-reproduction transition. The findings reveal a fundamental mechanism of nutrient signalling in direct epigenome reprogramming with broad relevance in the developmental control of multicellular organisms.
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影响因子:
12.3
作者:
Buels R;Yao E;Diesh CM;Hayes RD;Munoz-Torres M;Helt G;Goodstein DM;Elsik CG;Lewis SE;Stein L;Holmes IH
通讯作者:
Holmes IH
影响因子:
4.5
作者:
Bouyer D;Roudier F;Heese M;Andersen ED;Gey D;Nowack MK;Goodrich J;Renou JP;Grini PE;Colot V;Schnittger A
通讯作者:
Schnittger A
影响因子:
8.8
作者:
Forzani, Celine;Duarte, Gustavo T.;Meyer, Christian
通讯作者:
Meyer, Christian
影响因子:
64.8
作者:
Hsieh, Andrew C.;Liu, Yi;Edlind, Merritt P.;Ingolia, Nicholas T.;Janes, Matthew R.;Sher, Annie;Shi, Evan Y.;Stumpf, Craig R.;Christensen, Carly;Bonham, Michael J.;Wang, Shunyou;Ren, Pingda;Martin, Michael;Jessen, Katti;Feldman, Morris E.;Weissman, Jonathan S.;Shokat, Kevan M.;Rommel, Christian;Ruggero, Davide
通讯作者:
Ruggero, Davide
影响因子:
7.2
作者:
Clough, SJ;Bent, AF
通讯作者:
Bent, AF