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

Table 1 Genes involved in body length determination that were part of the present study.

Genotype	Allele	Protein	Pathway	Ref.
dbl-1	null	TGF-β growth factor	TGF-β	[44]
eat-1	unknown	α-actinin associated LIM protein	Feeding	[45]
eat-2	null	nicotinic acetylcholine receptor subunit	Feeding	[38]
eat-3	unknown	dynamin-like GTP binding protein	Feeding	[45]
eat-10	unknown	unknown	Feeding	[45]
egl-4	g.o.f*	cGMP dependent protein kinase	TGF-β	[45, 46]
kin-29	null	serine/threonine kinase	TGF-β	[47]
lon-1	e185* wk50*	PR (pathogenesis related)-protein	TGF-β	[48]
pha-2	l.o.f*	homeodomain transcription factor	Feeding	[39]
pha-3	unknown	unknown	Feeding	[45]
rnt-1	deletion*	RUNX transcription factor	not determined	[11]
sma-1	null	βH-spectrin	Spectrin	[6]
sma-2	missense*	TGF-β receptor signalling protein	TGF-β	[49]
sma-3	missense*	TGF-β receptor signalling protein	TGF-β	[49]
tax-6	missense**	serine/threonine protein phosphatase	Calcineurin	[9]

g.o.f* (gain of function alleles): egl-4(ad450) gain of function mutation, e185*: lon-1(e185) is considered to be a null allele. wk50*: lon-1(wk50) mutation cause a premature stop producing a 193 amino acid protein. l.o.f* (loss of function alleles): pha-2(ad472) is a pharynx specific loss of expression allele. Deletion*: in rnt-1(ok351) 38 amino acids are deleted, included parts of the DNA binding domain, mRNA is still produced. Missense*: both sma-2(e502) and sma-3(e491) contains missense mutations and the alleles are considered to be strong loss of function. Missense**: tax-6 (p675) is a missense mutation allele, complete or nearly loss of function

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