Temperature-dependent fasciation mutants connect mitochondrial RNA processing to control of lateral root morphogenesis

<jats:title>Abstract</jats:title><jats:p>Although mechanisms that activate organogenesis in plants are well established, much less is known about the subsequent fine-tuning of cell proliferation, which is crucial for creating properly structured and sized organs. Here we show, through analysis of temperature-dependent fasciation (TDF) mutants of Arabidopsis,<jats:italic>root redifferentiation defective 1</jats:italic>(<jats:italic>rrd1</jats:italic>),<jats:italic>rrd2</jats:italic>, and<jats:italic>root initiation defective 4</jats:italic>(<jats:italic>rid4</jats:italic>), that mitochondrial RNA processing is required for limiting cell division during early lateral root (LR) organogenesis. These mutants formed abnormally broadened (i.e., fasciated) LRs under high-temperature conditions due to excessive cell division. All TDF proteins localized to mitochondria, where they were found to participate in RNA processing: RRD1 in mRNA deadenylation, and RRD2 and RID4 in mRNA editing. Further analysis suggested that LR fasciation in the TDF mutants is triggered by reactive oxygen species generation caused by defective mitochondrial respiration. Our findings provide novel clues for the physiological significance of mitochondrial activities in plant organogenesis.</jats:p>