Bypass of Activation Loop Phosphorylation by Aspartate 836 in Activation of the Endoribonuclease Activity of Ire1.

Introduction of the D836A mutation into P-A-Ire1 further decreased expression of β-galactosidase 2 h after induction of ER stress with 2 mM DTT (from 11.2 ± 1.6 U/g to 5.6 ± 1.4 U/g) to levels very close to and statistically undistinguishable from levels seen in IRE1 deletion strains exposed to ER stress for 2 h (2.7 ± 0.4 U/g), but this decrease did not reach statistical significance.

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