부산대학교 도서관

SUMMARY: Proteostasis of the endoplasmic reticulum (ER) is controlled by sophisticated signaling pathways that are collectively called the unfolded protein response (UPR) and are initiated by specialized ER membrane‐associated sensors. The evidence that complete loss‐of‐function mutations of the most conserved of the UPR sensors, inositol‐requiring enzyme 1 (IRE1), dysregulates tissue growth and development in metazoans and plants raises the fundamental question as to how IRE1 is connected to organismal growth. To address this question, we interrogated the Arabidopsis primary root, an established model for organ development, using the tractable Arabidopsis IRE1 mutant ire1a ire1b, which has marked root development defects in the absence of exogenous stress. We demonstrate that IRE1 is required to reach maximum rates of cell elongation and root growth. We also established that in the actively growing ire1a ire1b mutant root tips the Target of Rapamycin (TOR) kinase, a widely conserved pro‐growth regulator, is hyperactive, and that, unlike cell proliferation, the rate of cell differentiation is enhanced in ire1a ire1b in a TOR‐dependent manner. By functionally connecting two essential growth regulators, these results underpin a novel and critical role of IRE1 in organ development and indicate that, as cells exit an undifferentiated state, IRE1 is required to monitor TOR activity to balance cell expansion and maturation during organ biogenesis. Significance Statement: Loss‐of‐function mutations of the conserved UPR regulator IRE1 cause developmental defects under physiological conditions of growth in Arabidopsis. Here, we show that in actively growing ire1a ire1b mutant root tips the TOR kinase, a widely conserved pro‐growth regulator, is hyperactive and that this hyperactivity leads to unbalanced rates of cell differentiation. Therefore, IRE1 is required to monitor TOR activity to balance cell expansion and maturation during root biogenesis. [ABSTRACT FROM AUTHOR]