L1 arrest

All organisms must cope with fluctuating nutrient availability by altering resource allocation between growth and survival. In order to accomplish this balancing act, physiological pathways must coordinately affect growth, development, metabolism and stress resistance. Like many animals, it is normal for the nematode C. elegans to face starvation in the wild, and so organismal fitness depends on developmental responses to nutrient availability. When C. elegans larvae hatch in the absence of food they arrest development and increase resistance to environmental stress (L1 arrest). Larvae in L1 arrest are not behaviorally quiescent but instead continue foraging and initiate development upon feeding. Using L1 arrest and recovery as a model, our research aims to identify and characterize signaling pathways and gene regulatory mechanisms that mediate developmental responses to nutrient availability (see links below).

Why do we study developmental physiology in a worm?

C. elegans is a powerful model system for studying development. Its benefits include a rapid generation time, invariant cell lineage, and compact genome as well as ever improving techniques for genetic and genomic analysis. Furthermore, its development is profoundly influenced by environmental conditions, and it is capable of phenotypic plasticity. The small size and relatively simple anatomy of the worm make it an excellent model to study signaling pathways that maintain organismal homeostasis during development. Though these signaling pathways tend to also affect aging, their developmental function is more likely to be adaptive. Maintaining homeostasis during development is critical to phenotypic robustness, and developmental physiology is therefore crucial to understanding the relationship of genotype to phenotype. This work is also relevant to cancer, since it addresses nutritional control of cell division and growth, and metabolic diseases like obesity and type II diabetes, which are increasingly common.