During the development of the C. elegans reproductive system, cells that give rise to the vulva, the vulval precursor cells (VPCs), remain quiescent for two larval stages before resuming cell division in the third larval stage. We have identified several transcriptional regulators that contribute to this temporary cell-cycle arrest. Mutation of lin-1 or lin-31, two downstream targets of the Receptor Tyrosine kinase (RTK)/Ras/MAP kinase cascade that controls VPC cell fate, disrupts the temporary VPC quiescence. We found that the LIN-1/Ets and LIN-31/FoxB transcription factors promote expression of CKI-1, a member of the p27 family of cyclin-dependent kinase inhibitors (CKIs). LIN-1 and LIN-31 promote cki-1/Kip-1 transcription prior to their inhibition through RTK/Ras/MAPK activation. Another mutation identified in the screen defined the mdt-13 TRAP240 Mediator subunit. Further analysis of the multi-subunit Mediator complex revealed that a specific subset of its components act in VPC quiescence. These components substantially overlap with the CDK-8 module implicated in transcriptional repression. Taken together, strict control of cell-cycle quiescence during VPC development involves transcriptional induction of CKI-1 and transcriptional regulation through the Mediator complex. These transcriptional regulators represent potential molecular connections between development and the basic cell-cycle machinery.