Abstract

BackgroundPlant plastidic caseinolytic protease (Clp) is a central part of the plastid protease network and consists of multiple subunits. The molecular functions of many Clps in plants, especially in crops, are not well known.ResultsIn this study, we identified an albino lethal mutant al3 in rice, which produces albino leaves and dies at the seedling stage. Molecular cloning revealed that AL3 encodes a plastid caseinolytic protease, OsClpR1, homologous to Arabidopsis ClpR1 and is targeted to the chloroplast. Compared with the wild type, chloroplast structure in the al3 mutant was poorly developed. OsClpR1 was constitutively expressed in all rice tissues, especially in young leaves. The OsClpR1 mutation affected the transcript levels of chlorophyll biosynthesis and chloroplast development-related genes. The RNA editing efficiency of three chloroplast genes (rpl2, ndhB, ndhA) was remarkably reduced in al3. Using a yeast two-hybrid screen, we found that OsClpR1 interacted with OsClpP4, OsClpP5, OsClpP2, and OsClpS1.ConclusionsCollectively, our results provide novel insights into the function of Clps in rice.

Highlights

  • Plant plastidic caseinolytic protease (Clp) is a central part of the plastid protease network and consists of multiple subunits

  • Using the yeast two-hybrid analysis, we found that OsClpR1 interacted with OsClpP4, OsClpP5, OsClpP2, and OsClpS1

  • The results showed that the green fluorescence of OsClpR1-GFP fully co-localized with the Chl fluorescence of the chloroplasts (Fig. 5b)

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Summary

Introduction

Plant plastidic caseinolytic protease (Clp) is a central part of the plastid protease network and consists of multiple subunits. The functional chloroplast is derived from the proplastid, and is synergistically regulated by the plastid and nuclear genomes (López-Juez 2007; Sakamoto et al 2008). The ATP-dependent Clp peptidase has been studied, and the plastid Clp proteolytic system in plants consists of five ClpP proteins, four ClpR proteins, and three Clp chaperones (ClpC1, ClpC2, and ClpD; Constan et al 2004; Sakamoto 2006; Sjögren and Clarke 2011). The ClpC1 knockout mutant exhibits growth retardation and leaf chlorosis, while there was no obvious phenotype in the clpC2 mutant (Zhang et al 2018). The leaves of the homozygous mutant osclpP5 were light yellow, and died at the three-leaf stage

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