AtIRE1A/AtIRE1B and AGB1 independently control two essential unfolded protein response pathways in Arabidopsis
Article first published online: 21 OCT 2011
DOI: 10.1111/j.1365-313X.2011.04788.x
© 2011 The Authors. The Plant Journal © 2011 Blackwell Publishing Ltd
Additional Information
How to Cite
Chen, Y. and Brandizzi, F. (2012), AtIRE1A/AtIRE1B and AGB1 independently control two essential unfolded protein response pathways in Arabidopsis. The Plant Journal, 69: 266–277. doi: 10.1111/j.1365-313X.2011.04788.x
Publication History
- Issue published online: 6 JAN 2012
- Article first published online: 21 OCT 2011
- Accepted manuscript online: 13 SEP 2011 03:06PM EST
- Received 2 August 2011; revised 6 September 2011; accepted 8 September 2011; published online 21 October 2011.
Keywords:
- unfolded protein response;
- inositol-requiring enzyme 1;
- GTP-binding protein β1;
- endoplasmic reticulum stress;
- root;
- Arabidopsis thaliana
Summary
The endoplasmic reticulum (ER) has the ability to maintain the balance between demand for and synthesis of secretory proteins. To ensure protein-folding homeostasis in the ER, cells invoke signaling pathways known as the unfolded protein response (UPR). To initiate UPR, yeasts largely rely on a conserved sensor, IRE1. In metazoans, there are at least three independent UPR signalling pathways. Some UPR transducers have been identified in plants, but no genetic interaction among them has yet been examined. The Arabidopsis genome encodes two IRE1 sequence homologs, AtIRE1A and AtIRE1B. Here we provide evidence that AtIRE1A and AtIRE1B have overlapping functions that are essential for the plant UPR. A double mutant of AtIRE1A and AtIRE1B, atire1a atire1b, showed reduced ER stress tolerance and a compromised UPR activation phenotype. We have also established that Arabidopsis AGB1, a subunit of the ubiquitous heterotrimeric GTP-binding protein family, and AtIRE1A/AtIRE1B independently control two essential plant UPR pathways. By demonstrating that atire1a atire1b has a short root phenotype that is enhanced by an agb1 loss-of-function mutation, we have identified a role for UPR transducers in organ growth regulation.

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