<i>TIC236</i> gain-of-function mutations unveil the link between plastid division and plastid protein import.

Abstract

SignificanceAlthough 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 <i>crumpled leaf</i> (<i>crl</i>) mutant deficient in plastid division led us to find dominant gain-of-function (GF) mutations in <i>TIC236</i>, which significantly increases the import of PDM components and completely rescues <i>crl</i> phenotypes. The defective plastid division phenotypes in <i>crl</i> and <i>tic236-knockdown</i> 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.