[대학원 생명과학과 세미나 안내]
연사 : 김찬홍 교수(Chinese Academy of Sciences)
연제 : From singlet oxygen signaling to chloroplast protein import pathways: An unforeseen adventure
일시 : 2021년 03월 26일 (금) 오후 5시
장소 : 온라인 화상 강의로 진행됩니다.
초청교수 : 오은규 교수
Abstract
Chloroplast-generated singlet oxygen (1O2), a ROS mainly produced by PSII, alters nuclear transcriptome via retrograde signaling pathways (Dogra et al., 2019), contributing to foliar acclimation and cell death responses. An Arabidopsis crumpled leaf (crl) mutant deficient in plastid binary fission is known to express 1O2-responsive nuclear genes constitutively. The crl gigantic chloroplasts induce autoimmune responses through lipid peroxidation-dependent retrograde signaling (Li et al., 2020). In the present study, via a forward genetic screen, we unveil dominant gain-of-function TRANSLOCON AT THE INNER ENVELOPE OF CHLOROPLAST (TIC236) mutations, each of which abolishes the autoimmune responses and rescues the plastid-division defect in crl. This result indicates the shared functionality between CRL (mainly located in the outer envelope of chloroplast) and TIC236 proteins. Ensuing reverse genetic analyses show CRL's genetic interaction with SP1, a RING-type ubiquitin E3 ligase (Ling et al., 2012), and the intrinsic inner envelope membrane FTSH11 protease (Adam et al., 2019), whose functions are implicated in TOC and TIC turnover, respectively. Either loss of SP1 or FTSH11 rescues crl phenotypes in varying degrees due to increased translocon levels. Consistent with the impaired plastid division in both crl and tic236-knockdown mutants, CRL interacts with the preproteins of plastid-division machinery, and TIC236GF reinforces their import. Last but not least, we found these GF mutations significantly stabilize TIC236 proteins. We collectively shed new light on the probable link between protein import defect and plant innate immunity.