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. 2010 Mar-Apr;101(Suppl 1):S62–S74. doi: 10.1093/jhered/esq003

Table 1.

Mutations with effects on mating system dynamics in Caenorhabditis elegans

Gene Function Mating system effect Functional background Evolutionary applications
fog-2 F-box protein that binds tra-2 mRNA before sexual maturity, thereby initiating germ-line production of sperm in hermaphrodites. Mutants do not undergo protandrous production of sperm, effectively feminizing hermaphrodites, leading to dioecy and obligate outcrossing. Schedl and Kimble (1988); Clifford et al. (2000); Nayak et al. (2005) Stewart and Phillips (2002); Katju et al. (2008); Morran, Parmenter, et al. (2009)
him-5 Influences the number and distribution of X chromosome pairing events; molecular function currently unknown. Causes X-specific nondisjunction and so leads to high frequency of males. Hodgkin et al. (1979); Broverman and Meneely (1994) Chasnov and Chow (2002); Cutter and Payseur (2003)
spe-8 Protein tyrosine kinase involved in the sperm activation signaling pathway. Produces nonfunctional sperm in hermaphrodites, leading to dioecy. L'Hernault et al. (1988); Muhlrad and Ward (2002) LaMunyon and Ward (2002); LaMunyon et al. (2007)
spe-26 Actin-binding protein needed for normal spermatogenesis. Effects as in spe-8. Varkey et al. (1995); Minniti et al. (1996) Cutter (2005)
tra-2 Membrane-bound protein that controls trafficking of the sex determination signaling pathway. Mutants transform hermaphrodites into males. A temperature-sensitive version can be used to mimic temperature-dependent sex determination, such as that found in turtles. Hodgkin and Brenner (1977); Kuwabara et al. (1992); Kuwabara and Kimble (1995); Hodgkin (2002) Janzen and Phillips (2006); Chandler et al. (2009)
tra-3 Regulatory protease that cleaves tra-2. Can delay the transition between sperm and egg production in hermaphrodites, thereby shifting the pattern of sex allocation. Hodgkin and Brenner (1977); Sokol and Kuwabara (2000) Hodgkin and Barnes (1991)
xol-1 Metabolic kinase that helps assess the X/autosome ratio and regulates X chromosome dosage compensation. Mutants disrupt dosage compensation, which leads to male (XØ) lethality and results in obligate selfing. Miller et al. (1988); Rhind et al. (1995) Morran, Parmenter, et al. (2009)