"We crossed the
lin-65(
n3441) mutation into animals harboring a reporter (
hsp-4p::gfp) for an ER-specific stress response, the UPRer (Ron and Walter, 2007). Animals were then treated with the ER-specific stressor tunicamycin, which blocks N-linked glycosylation and induces the UPRer (Heifetz et al., 1979).
lin-65 did not affect the upregulation of the
hsp-4p::gfp reporter by tunicamycin (Figure S1C)."