SUMO protease FUG1, histone reader AL3 and chromodomain protein LHP1 are integral to repeat expansion-induced gene silencing in Arabidopsis thaliana

被引：4

作者：

Sureshkumar, Sridevi ^{[1
]}

Bandaranayake, Champa ^{[1
]}

Lv, Junqing ^{[2
]}

Dent, Craig I. ^{[1
]}

Bhagat, Prakash Kumar ^{[3
]}

Mukherjee, Sourav ^{[1
]}

Sarwade, Rucha ^{[1
]}

Atri, Chhaya ^{[1
]}

York, Harrison M. ^{[4
,5
]}

Tamizhselvan, Prashanth ^{[1
]}

Shamaya, Nawar ^{[1
]}

Folini, Giulia ^{[1
]}

Bergey, Benjamin G. ^{[6
]}

Yadav, Avilash Singh ^{[1
]}

Kumar, Subhasree ^{[1
]}

Grummisch, Oliver S. ^{[1
]}

Saini, Prince ^{[7
]}

Yadav, Ram K. ^{[7
]}

Arumugam, Senthil ^{[4
,5
]}

Rosonina, Emanuel ^{[6
]}

Sadanandom, Ari ^{[3
]}

Liu, Hongtao ^{[2
]}

Balasubramanian, Sureshkumar ^{[1
]}

机构：

[1] Monash Univ, Sch Biol Sci, Clayton Campus, Melbourne, Vic, Australia

[2] Chinese Acad Sci, CAS Ctr Excellence Mol Plant Sci, Inst Plant Physiol & Ecol, Natl Key Lab Plant Mol Genet, Shanghai, Peoples R China

[3] Univ Durham, Dept Biosci, Durham, England

[4] Monash Univ, Fac Med Nursing & Hlth Sci, Monash Biomed Discovery Inst, Clayton Campus, Melbourne, Vic, Australia

[5] Monash Univ, European Mol Biol Lab, Australia EMBL Australia, Clayton Campus, Melbourne, Vic, Australia

[6] York Univ, Dept Biol, Toronto, ON, Canada

[7] Indian Inst Sci Educ & Res, Dept Biol Sci, Mohali, India

来源：

NATURE PLANTS | 2024年 / 10卷 / 05期

基金：

澳大利亚研究理事会; 英国医学研究理事会;

关键词：

NATURAL VARIATION; SUMOYLATION SITES; PREDICTION; NUCLEUS; FINGER; STRESS; SENP7; TOOL;

D O I：

10.1038/s41477-024-01672-5

中图分类号：

Q94 [植物学];

学科分类号：

071001 ;

摘要：

Epigenetic gene silencing induced by expanded repeats can cause diverse phenotypes ranging from severe growth defects in plants to genetic diseases such as Friedreich's ataxia in humans. The molecular mechanisms underlying repeat expansion-induced epigenetic silencing remain largely unknown. Using a plant model with a temperature-sensitive phenotype, we have previously shown that expanded repeats can induce small RNAs, which in turn can lead to epigenetic silencing through the RNA-dependent DNA methylation pathway. Here, using a genetic suppressor screen and yeast two-hybrid assays, we identified novel components required for epigenetic silencing caused by expanded repeats. We show that FOURTH ULP GENE CLASS 1 (FUG1)-an uncharacterized SUMO protease with no known role in gene silencing-is required for epigenetic silencing caused by expanded repeats. In addition, we demonstrate that FUG1 physically interacts with ALFIN-LIKE 3 (AL3)-a histone reader that is known to bind to active histone mark H3K4me(2/3). Loss of function of AL3 abolishes epigenetic silencing caused by expanded repeats. AL3 physically interacts with the chromodomain protein LIKE HETEROCHROMATIN 1 (LHP1)-known to be associated with the spread of the repressive histone mark H3K27me(3) to cause repeat expansion-induced epigenetic silencing. Loss of any of these components suppresses repeat expansion-associated phenotypes coupled with an increase in IIL1 expression with the reversal of gene silencing and associated change in epigenetic marks. Our findings suggest that the FUG1-AL3-LHP1 module is essential to confer repeat expansion-associated epigenetic silencing and highlight the importance of post-translational modifiers and histone readers in epigenetic silencing.

引用

页码：749 / 759

页数：22