Thermotolerance of an organism is a complex trait that is influenced by a multitude of genetic and environmental factors. Many factors controlling thermotolerance in <i>Caenorhabditis elegans</i> are known to extend life. To understand the regulation of thermotolerance, we performed a genetic screen for mutants with better survival at warm temperature. Here we identified by dauer survival a <i>
tax-2</i> mutation and several mutations disrupting an insulin signaling pathway including the <i>
daf-2</i> gene. While the <i>
tax-2</i> mutant has improved thermotolerance and long life span, the newly identified <i>
daf-2</i> and other insulin signaling mutants, unlike the canonical <i>
daf-2(
e1370)</i>, do not show improved thermotolerance despite being long-lived. Examination of <i>
tax-2</i> mutations and their mutant phenotypes suggest that the control of thermotolerance is not coupled with the control of life span or dauer survival. With genetic interaction studies, we concluded that <i>
tax-2</i> has complex roles in life span and dauer survival and that <i>
tax-2</i> is a negative regulator of thermotolerance independent of other known thermotolerance genes including those in the insulin signaling pathway. Moreover, cold growth temperature during development weakens the improved thermotolerance associated with <i>
tax-2</i> and other thermotolerance-inducing mutations. Together, this study reveals previously unknown genetic and environmental factors controlling thermotolerance and their complex relationship with life span regulation.