Worm Breeder's Gazette 15(3): 30 (June 1, 1998)
These abstracts should not be cited in bibliographies. Material contained herein should be treated as personal communication and should be cited as such only with the consent of the author.
|1||Dept. of Biochemistry and HHMI, Columbia University College of Physicians and Surgeons, NY, NY 10032|
|2||Current address: Dept. of Biology, NYU, NY, NY 10003|
lin-12(n941) is an EMS-induced lin-12 allele that our lab uses as the canonical null allele for genetic studies. This allele contains an amber stop codon in the eighth EGF-like motif (amino acid W400STOP). This observation suggests that lin-12(n941) is a molecular null allele. lin-12(n941) causes a highly penetrant 2 AC defect and other cell fate transformations as described in Greenwald et al. (1983). Note that in the presence of smg-1, the lin-12(n941) allele causes an embryonic lethal phenotype, probably as a result of a dominant-negative effect of the truncated extracellular domain (Hilary Wilkinson, personal communication.) lin-12(n302ar220) behaves like a null allele; it contains a UV/TMP-induced lesion, ar220, a small deletion in the extracellular domain that creates a frameshift mutation in the fourth EGF-like motif. We have not examined the effect of smg-1 on this allele. lin-12(n676n930) is an EMS-induced hypomorphic allele that we have used for many genetic studies in our lab. This allele contains a missense mutation in the second EGF-like repeat (amino acid C138Y). The genetic properties of this allele have been described in detail in Sundaram and Greenwald (1993a). Sequence changes associated with lin-12(n302), lin-12(n676) and most other lin-12(d) mutations were published in Greenwald and Seydoux (1990).