Yellow barley xan-m mutants are deficient in the motor unit SECA1 of the SEC1 translocase system.

Abstract

Main conclusion: Chloroplast protein transport depends on the SEC1 translocase. Barley xan-m mutants, deficient in SECA1, lack chlorophyll and die as seedlings. Their yellow phenotype indicates that carotenoid chemistry is less SEC1-dependent. Chloroplast proteins encoded by genes located in the cell nucleus need to be transported across up to three chloroplast membranes to find its correct location. SEC1 is one of the major translocase systems. In plants, SEC1 consists of three proteins (SECA1, SECY1 and SECE1) and transports substrate proteins over the thylakoid membrane. SECA1 is an ATPase that delivers the substrate protein to the SECY1-SECE1 channel. In the present study, we analyzed five allelic barley xan-m mutants, which had been isolated between 1925 and 1957. The mutants belong to a larger collection of barley mutants deficient in chlorophyll biosynthesis and chloroplast development. Mutations in the xan-m gene are recessive and result in a yellow phenotype due to lack of chlorophyll and presence of carotenoids. Mutant seedlings die after approximately 10 days. We identified the defective gene in the xan-m mutants by a variant of bulk segregant analysis. The gene xan-m is an orthologue of SECA1 in Arabidopsis. Previously, only genes related to chlorophyll biosynthesis have been identified in the collection of barley xan mutants. The yellow phenotype of the mutants demonstrates that proteins responsible for carotenoid biosynthesis and storage are not or less dependent on an intact SEC1 translocase.