Timing is crucial to development: an embryo needs to make the right tissues at the right times, and also to coordinate developmental events in different tissues. Heterochronic shifts in development result in changes of relative timing of developmental events, and the genetic control of this process has been most thoroughly investigated in C. elegans. One crucial heterochronic gene is lin-28, mutants of which display precocious larval development; however, the broader role of lin-28 in inter-tissue coordination is incompletely understood, and is the focus of Sungwook Choi and Victor Ambros’ current study. The authors first show that lin-28 mutant hermaphrodites produce fewer larval progeny, due to reduced embryo production and lower embryonic viability. Fertilised embryos become trapped inside the gonadal spermathecal, most likely due to abnormalities in the Sp-Ut valve through which fertilised embryos transit to the uterus. Maternally provided LIN-28 can rescue embryonic lethality, and although the same genetic network downstream of lin-28 functions in the hypodermis and the gonad, the temporal developmental coordination of these two tissues is lost in mutant worms. Finally, hypodermal, but not somatic gonadal, expression of lin-28 is sufficient to restore gonadal morphology, and consequently to restore embryonic viability. Thus, developmental coordination between the hypodermis and the gonad is regulated by a hypodermal heterochronic gene and is crucial for fertility.
