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Background  Mutations that cause feeding defects in the nematode  C. elegans  are known to increase life span. Here we show that feeding defective mutants also have a second general trait in common, namely that they are small.    Results  Our measurements of the body lengths of a variety of feeding defective mutants, or of a variety of double mutants affecting other pathways that regulate body length in  C. elegans , i.e. the DBL-1/TGFβ, TAX-6/calcineurin and the SMA-1/β H -spectrin pathways, indicate that food uptake acts as a separate pathway regulating body length. In early stages, before eating begins, feeding defective worms have no defect in body length or, in some cases, have only slightly smaller body length compared to wild-type. A significant difference in body length is first noticeable at later larval stages, a difference that probably correlates with increasing starvation. We also show that autophagy is induced and that the quantity of fat is decreased in starved worms.    Conclusion  Our results indicate that the long-term starvation seen in feeding-defective  C. elegans  mutants activates autophagy, and leads to depletion of fat deposits, small cell size and small body size.

C. elegansfeeding defective mutants have shorter body lengths and increased autophagy