Temperature is perceived primarily via transient receptor potential (TRP) channels, which are integral to the molecular machinery sensing environmental and cellular signals. Functional evidence of TRP channels' involvement in regulating cold-induced developmental/reproductive responses remains scarce. Here, we show that mutations affecting cold-sensing TRP channels antagonize the reduction in ovarian development induced by low temperatures (reproductive dormancy) in . More specifically, mutants for , , and significantly lowered dormancy levels at 12 °C and exhibited well-developed oocytes characterized by advanced vitellogenesis. Similarly, functional knockouts for , a gene encoding a phospholipase C acting downstream to Trp and Trpl, exhibited a reduced dormancy response, suggesting that Ca signaling is key to relaying cold-sensing stimuli during dormancy induction and maintenance. Finally, mutants with an altered temperature preference (i.e., exhibiting impaired cold or warm avoidance) differentially responded to the cold, either lowering or increasing dormancy levels. In summary, our phenotypic analysis provides functional evidence of developmental/reproductive modulation by specific cold-sensing TRP channels in and indicates that temperature preference affects developmental processes.