Ectopic expression of the germline transcription factor LSL-1 contributes to developmental delay following failed maternal epigenetic reprogramming

In this study, we investigated how the germline transcription factor LSL-1 contributes to developmental defects caused by failed maternal epigenetic reprogramming in Caenorhabditis elegans. We found that LSL-1 becomes ectopically expressed in somatic tissues of spr-5; met-2 mutants and that depletion of LSL-1 partially rescues their developmental delay.

RNA-seq analyses showed extensive overlap between MES-4- and LSL-1-dependent transcriptional programs and revealed that ectopic lsl-1 expression itself depends on MES-4. These findings identify LSL-1 as a downstream effector of MES-4 that promotes aberrant germline-associated transcription and developmental delay.