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

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

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]
  1. 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