Figure 2.

Model of body size regulation by nutrients availability in C. elegans (from L3 onwards). Our results suggest that food availability may regulate body size in at least two ways. First, by the "caloric pathway", that is, simply considering that food intake and its absorption by the digestive tract facilitates nutrition, which in turn may inhibit autophagy. Second, by the "sensory pathway", which refers to the sensing food through organs such as the amphids, with their ciliated neurons expressing genes like che-2, would inhibit EGL-4. Downstream, this cGMP-dependent protein kinase downregulates DBL-1 signalling, which in turn promotes hypodermal endoreduplication, upregulator of body size [36]. LON-1 inhibition by DBL-1 [28] would not influence ploidy upon nutrient activation. This model explains why the nutrient-dependent regulation that the sensory cilia proteins, EGL-4 and DBL-1 are all playing on hypodermal polyploidization has not been observed for body size; their role on body size, but not upon endoreduplication, may be obscured by the dominant influence of caloric restriction.

Tain et al. BMC Developmental Biology 2008 8:28   doi:10.1186/1471-213X-8-28
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