Non-apoptotic death of the C. elegans linker cell is primed by MYRF-1 activation of pqn-41/polyQ
Yarychkivska, O.; Liu, S.; Horowitz, L. B.; Newland, S.; Wu, P.; Mittal, S.; Tamura, S.; Novosolova, T.; Ritter, D. F.; Lu, Y.; Ercan, S.; Hammell, C.; Shaham, S.
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Linker cell-type death (LCD) is a morphologically conserved non-apoptotic cell-death process with features resembling polyglutamine-dependent neurodegeneration. In C. elegans development, LCD eliminates the male-specific linker cell following its long-range migration. Using single-cell mRNA sequencing of migrating and dying linker cells, we identify myrf-1, encoding a membrane-bound transcription factor implicated in human developmental disorders, as a key LCD regulator. MYRF-1 translocates to the linker cell nucleus during early migration and, surprisingly, its auxin-inducible degradation then, but not later, blocks LCD. MYRF-1 directly binds known LCD genes, including pqn-41, encoding an aggregation-prone polyglutamine protein. Deleting a bona fide MYRF-1-binding site within pqn-41 promotes linker cell survival. Our findings reveal that linker cell death is primed well before cell demise takes place, temporally uncoupling death commitment and execution.
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