SynMuv genes and alleles

GeneNo. of allelesMutant allelesProbable null phenotype (evidence)
Class A
        lin-8 9 n111, n2376, n2378, n2403, n2724, n2731, n2738, n2739, n2741 SynMuva (no. alleles)
    lin-15A13 n433, n749, n767, n2375, n2725, n2726, n2733, n2734, n2735, n2737, n2742, sy211, sy212 SynMuv (molecular datab, no. alleles)
        lin-38 4 n751, n761, n2402, n2727 Unknown
        lin-56 1 n2728 Unknown
Class B
        lin-9 3 n112, n942, n943 SynMuv, sterile (molecular datac, non-complementation screend)
        lin-13 8n770, n2238, n2981, n2984, n2985, n2988 (n387 and possibly n388 at 15°d)SynMuv, sterile, maternal-effect lethala (molecular datae)
    lin-15B14 n374, n743, n744, n2230, n2233, n2241, n2244, n2245, n2980, n2983, n2987, n2989, n2991, n2993 SynMuv (molecular datab, no. alleles)
        lin-35 8 n373, n745, n2232, n2236, n2239, n2242, n2977, n2996 SynMuv (molecular dataf, no. alleles)
        lin-36 13 n747, n750, n766, n772, n2235, n2240, n2243, n3090, n3093, n3094, n3095, n3096, n3097 SynMuv (molecular datag, noncomplementation screeng)
        lin-37 2 n758, n2234 SynMuv (molecular datah)
        lin-52 2 n771, n3718 SynMuv, sterile (molecular datai)
        lin-53 3 n833, n2978, n3368j SynMuv, sterile, protruding vulva (molecular dataj, n833 and n2978 are dominant negativek)
        lin-54 2 n2231, n2990 Unknown
        dpl-1 4 n2994, n3316, n3643, zu355 SynMuv, sterile, maternal-effect lethal (phenotype enhanced by Df, molecular datal, zu355 isolated in maternal-effect lethal screenm)
        tam-1n 18cc566, cc567, cc587, sy272, and 14 othersSynMuv (molecular datao, no. alleleso, phenotype not enhanced by Dfo)
        let-418 3 ar113, ar114, s1617 SynMuv, sterile, maternal-effect lethal, everted vulva (molecular datap, phenotype not enhanced by Dfp)
        efl-1 3 n3318, n3639, se1 SynMuv, sterile, maternal-effect lethalq(molecular datal, se1 isolated in maternal-effect lethal screenm)
        hda-1 1 e1795r SynMuv, protruding vulva, gonad development abnormal and sterile (molecular datas)
        mep-1 1 q660 SynMuvt,u, sterilet,v, protruding vulvat,v, larval lethalv (molecular datat,v)

Mutant alleles not described in the text are described by Horvitz and Sulston (1980), Ferguson and Horvitz (1985, 1989), Desai et al. (1988), Huang et al. (1994), Thomas and Horvitz (1999), Hsieh et al. (1999), Von Zelewsky et al. (2000), Ceol and Horvitz (2001), and Page et al. (2001). Probable null phenotype is given at 20°; see Table 1. Under evidence, no. alleles indicates that a high number of mutations were isolated in the screens described in the text, consistent with the hypothesis that some of these alleles are null alleles.

  • a See Ferguson and Horvitz (1985) for possibly contradictory deficiency data.

  • b Clark et al. (1994); Huang et al. (1994).

  • c Beitel et al. (2000).

  • d Ferguson and Horvitz (1989).

  • e Melendez and Greenwald (2000).

  • f Lu and Horvitz (1998).

  • g Thomas and Horvitz (1999).

  • h Lu (1999).

  • i See text.

  • j X. Lu and H. R. Horvitz (personal communication).

  • k Text and Lu and Horvitz (1998).

  • l Ceol and Horvitz (2001).

  • m Page et al. (2001).

  • n This gene does not act as a class B synMuv in double mutants with lin-8, but does with lin-15A and lin-38 (Hsieh et al. 1999). Such an interaction had not been previously observed for the synMuv genes, but lin-8(n111) synMuv double mutants have occasionally been observed to be weaker than corresponding synMuv double mutants carrying other class A mutations (Thomas and Horvitz 1999).

  • o Hsieh et al. (1999).

  • p Von Zelewsky et al. (2000).

  • q Page et al. (2001); C. J. Ceol and H. R. Horvitz (unpublished results).

  • r hda-1 is also known as gon-10 (Dufourcq et al. 2002). The hda-1(e1795) mutation alone causes a weakly penetrant Muv phenotype (Dufourcq et al. 2002), but in combination with the class A mutation lin-15(n767) this phenotype is fully penetrant and displays stronger expressivity (C. J. Ceol, E. C. Andersen and H. R. Horvitz, unpublished results).

  • s Dufourcq et al. (2002).

  • t (C. J. Ceol, F. Stegmeier, M. M. Harrison and H. R. Horvitz, unpublished results).

  • u Unhavaithaya et al. (2002).

  • v Belfiore et al. (2002).