SMALL KERNEL4is required for mitochondrial cox1 transcript editing and seed development in maize.

Abstract

In land plants, cytidine-to-uridine (C-to-U) editing of organellar transcripts is an important post-transcriptional process, which is considered to remediate DNA genetic mutations to restore the coding of functional proteins. Pentatricopeptide repeat (PPR) proteins have key roles in C-to-U editing. Owing to its large number, however, the biological functions of many PPR proteins remain to be identified. Through characterizing a small kernel4 (smk4) mutant, here we report the function of Smk4 and its role in maize growth and development. Null mutation of Smk4 slows plant growth and development, causing small plants, delayed flowering time, and small kernels. Cloning revealed that Smk4 encodes a new E-subclass PPR protein, and localization indicated that SMK4 is exclusively localized in mitochondria. Loss of Smk4 function abolishes C-to-U editing at position 1489 of the cytochrome c oxidase1 (cox1) transcript, causing an amino acid change from serine to proline at 497 in Cox1. Cox1 is a core component of mitochondrial complex IV. Indeed, complex IV activity is reduced in the smk4, along with drastically elevated expression of alternative oxidases (AOX). These results indicate that SMK4 functions in the C-to-U editing of cox1-1489, and this editing is crucial for mitochondrial complex IV activity, plant growth, and kernel development in maize.