endoplasmic reticulum stress vulnerability in haploid human somatic cells

Haploid cells exhibit higher protein aggregation even in unperturbed conditions.

ER stress-driven haploid instability stems from inefficient proteostatic control that alters UPR functionality to cause apoptosis selectively in haploids.

Haploidy-linked vulnerability to ER stress is a critical cause of haploid intolerance in human somatic cells.

Upon ER stress induction, UPR activation dynamics are similar in haploid and diploid cells, but haploid cells are less efficient at resolving proteotoxic stress and are biased toward proapoptotic UPR signaling.

Pharmacological induction of ER stress selectively induces apoptosis in haploid cells and facilitates their replacement by coexisting diploidized cells in a caspase-dependent manner.

Long-term stability of the haploid state is improved by alleviating natural proteotoxicity.