Open AccessTIC236 gain-of-function mutations unveil the link between plastid division and plastid protein import
Author(s) -
Jun Fang,
Bingqi Li,
LihJen Chen,
Vivek Dogra,
Shengji Luo,
Wangpin Wu,
Pengcheng Wang,
Inhwan Hwang,
Hsoumin Li,
Kim C
Publication year - 2022
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.2123353119
Subject(s) - plastid , biology , mutant , genetics , mutation , cell division , division (mathematics) , function (biology) , microbiology and biotechnology , gene , chloroplast , cell , arithmetic , mathematics
Significance Although plastid division is critical for plant development, how components of the plastid division machinery (PDM) are imported into plastids remains unexplored. A forward genetic screen to identify suppressors of acrumpled leaf (crl ) mutant deficient in plastid division led us to find dominant gain-of-function (GF) mutations inTIC236 , which significantly increases the import of PDM components and completely rescuescrl phenotypes. The defective plastid division phenotypes incrl andtic236-knockdown mutants and CRL-TIC236 association in a functional complex indicate that the CRL-TIC236 module is vital for plastid division. Hence, we report the first GF translocon mutants and unveil CRL as a novel functional partner of TIC236 for PDM import.