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Abstract

Developmental plasticity plays critical roles in the adaptation of many species and
has been proposed to facilitate phenotypic evolution. One of few examples where
genetic control of developmental plasticity is well-understood is dauer formation in
C. elegans. Dauer is an arrested larval stage in nematodes that is specialized for
survival and dispersal. In response to cues that indicate stressful environments, C.
elegans redirects its development to form stress-resistant dauer larvae. Genetic
control of C. elegans dauer formation is extensively studied and so far more than
20 genes are known to be involved in this process. To address how the genetic
control of dauer formation evolved, I set out to study the regulation of dauer
formation in a genetically tractable nematode Pristionchus pacificus. I found among
the mechanisms involved in C. elegans dauer formation, an endocrine module
employing a steroid hormone, dafachronic acid (DA), is conserved in P. pacificus
dauer formation. The same endocrine mechanism is found to be also involved in the
regulation of mouthform dimorphism that is a novel plastic trait in Pristionchus and
related nematodes. Furthermore, DA is conserved in a parasitic nematode
(Strongyloides papillosus) to regulate the formation of the infective larva that is a
dauer-like larva essential for the host infection. These results suggest DA is a
conserved steroid hormone for the regulation of developmental plasticity in
nematodes. Implications of these findings for the evolution of nematode parasitism
will be discussed.