ABSTRACTImpaired plastid translation affects various aspects of plant development, but the molecular mechanism remains elusive. Here, we described that the reduced function of plastid translation elongation factor EF-Tu encoded by RAB GTPASE HOMOLOG 8D (Rab8d) elicits defects in root development, including the reduced meristem size, programmed cell death (PCD) in the stem cell niche (SCN), and quiescent center (QC) division. We found that the ATAXIA-TELANGIECTASIA-MUTATED (ATM)-SUPPRESSOR OF GAMMA RESPONSE 1 module mediated overexpression of SIAMSE-RELATED 5 in the root meristem region is responsible for the reduced meristem size in the rab8d mutant through arresting the cell cycle. The QC activation in rab8d is dependent on ETHYLENE RESPONSE FACTOR 115, which expression is tightly associated with the PCD in SCN. We further found that Rab8d physically interacts with GENOME UNCOUPLED 1 (GUN1), and GUN1 is required for inducing PCD in the rab8d SCN. However, the loss of GUN1 function in rab8d severely impairs the root architecture, suggesting that the GUN1-mediated renewal of stem cells is essential for maintaining root growth. Our observations extend our knowledge on the roles of ATM and GUN1 in regulating root development through mediating plastid translation dependent signals.One-sentence summaryThe rab8d-dependent plastid signal mediated by ATM and GUN1 regulates the root meristem size and renewal of root stem cells, respectively.
Plastid EF-Tu Regulates Root Development through Both the ATM Pathway and GUN1
