Journal
LIFE SCIENCE ALLIANCE
Volume 2, Issue 5, Pages -Publisher
LIFE SCIENCE ALLIANCE LLC
DOI: 10.26508/lsa.201900459
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Funding
- Ministry of Education, Culture, Sports, Science and Technology (MEXT) [26450010, 17K07610]
- Shorai Foundation for Science and Technology
- Takeda Science Foundation
- Grants-in-Aid for Scientific Research [17K07610, 26450010] Funding Source: KAKEN
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In Arabidopsis, the IRE1A and IRE1B double mutant (ire1a/b) is unable to activate cytoplasmic splicing of bZIP60 mRNA and regulated IRE1-dependent decay under ER stress, whereas the mutant does not exhibit severe developmental defects under normal conditions. In this study, we focused on the Arabidopsis IRE1C gene, whose product lacks a sensor domain. We found that the ire1a/b/c triple mutant is lethal, and heterozygous IRE1C (ire1c/) mutation in the ire1a/b mutants resulted in growth defects and reduction of the number of pollen grains. Genetic analysis revealed that IRE1C is required for male gametophyte development in the ire1a/b mutant background. Expression of a mutant form of IRE1B that lacks the luminal sensor domain (ALB) complemented a developmental defect in the male gametophyte in ire1a/b/c haplotype. In vivo, the ALE , protein was activated by glycerol treatment that increases the composition of saturated lipid and was able to activate regulated IRE1-dependent decay but not bZ1P60 splicing. These observations suggest that IRE1 contributes to plant development, especially male gametogenesis, using an alternative activation mechanism that bypasses the unfolded protein-sensing luminal domain.
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