TIC236 gain-of-function mutations unveil the link between plastid division and plastid protein import.
TIC236 gain-of-function mutations unveil the link between plastid division and plastid protein import.
复制标题
TIC236功能获得突变揭示了质体分裂和质体蛋白输入之间的联系
DOI：
10.1073/pnas.2123353119
复制
发表时间：
2022-03-15
影响因子：
11.1
通讯作者：
Kim C
中科院分区：
文献类型：
--
作者：
Fang J;Li B;Chen LJ;Dogra V;Luo S;Wu W;Wang P;Hwang I;Li HM;Kim C
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 a crumpled leaf (crl) mutant deficient in plastid division led us to find dominant gain-of-function (GF) mutations in TIC236, which significantly increases the import of PDM components and completely rescues crl phenotypes. The defective plastid division phenotypes in crl and tic236-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. TIC236 is an essential component of the translocon for protein import into chloroplasts, as evidenced by the embryonic lethality of the knockout mutant. Here, we unveil a TIC236-allied component, the chloroplast outer membrane protein CRUMPLED LEAF (CRL), absence of which impairs plastid division and induces autoimmune responses in Arabidopsis thaliana. A forward genetic screen exploring CRL function found multiple dominant TIC236 gain-of-function (tic236-gf) mutations that abolished crl-induced phenotypes. Moreover, CRL associates with TIC236, and a tic236-knockdown mutant exhibited multiple lesions similar to the crl mutant, supporting their shared functionality. Consistent with the defective plastid division phenotype of crl, CRL interacts with the transit peptides of proteins essential in plastid division, with tic236-gf mutations reinforcing their import via increased TIC236 stability. Ensuing reverse genetic analyses further revealed genetic interaction between CRL and SP1, a RING-type ubiquitin E3 ligase, as well as with the plastid protease FTSH11, which function in TOC and TIC protein turnover, respectively. Loss of either SP1 or FTSH11 rescued crl mutant phenotypes to varying degrees due to increased translocon levels. Collectively, our data shed light on the links between plastid protein import, plastid division, and plant stress responses.
登录
查看更多内容
影响因子：
7.2
作者：
Constan, D;Patel, R;Jarvis, P
通讯作者：
Jarvis, P
PSII 蛋白质稳态受损会在拟南芥 var2 突变体中引发类似 UPR 的反应
影响因子：
6.9
作者：
Dogra, Vivek;Duan, Jianli;Kim, Chanhong
通讯作者：
Kim, Chanhong
拟南芥巨型叶绿体突变体需要脂肪酸去饱和酶5诱导自身免疫反应
影响因子：
11.6
作者：
Li, Bingqi;Fang, Jun;Kim, Chanhong
通讯作者：
Kim, Chanhong
死亡还是不死？病变模仿突变体的教训。
影响因子：
5.6
作者：
Bruggeman Q;Raynaud C;Benhamed M;Delarue M
通讯作者：
Delarue M
TIC20和TIC22是叶绿体内膜膜上蛋白质进口设备的新成分。
影响因子：
7.8
作者：
Kouranov, A;Chen, X;Fuks, B;Schnell, D J
通讯作者：
Schnell, D J