Worm Breeder's Gazette 7(1): 45
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lin-14. In the last newsletter (Vol. 6, No. 1), we described heterochronic mutants that define the gene lin-14. Gene dosage experiments have indicated that the dominant lin-14 alleles, which cause reiteration of early larval characteristics, are hypermorphic ( cause elevated levels of wild-type lin-14 function); the recessive alleles, which cause the deletion of early larval developmental events and precocious expression of later events, are hypomorphic or amorphic (cause reduced or eliminated lin-14 function). These observations support the hypothesis that the level of lin-14 function determines the cell fates of certain cells: high lin-14 levels define events that occur early during wild-type postembryonic development, and low levels define later events. Although most recessive lin-14 alleles are pleiotropic and fail to complement each other for all defects, several of these defects are independently mutable: 16 alleles delete L1- specific cell divisions of the lateral hypodermis, with precocious expression of subsequent stages; three alleles have normal L1 development, but L2-specific divisions are deleted and L3 and L4 divisions are precocious; one mutant, isolated by Meredith Kusch, has normal L1, L2 and L3 development, but the lateral hypodermal seam cells form adult alae one stage earlier than in wild type. This independent mutability of the timing of adult alae formation and of the lateral hypodermal cell lineage pattern is further exemplified by another lin-14 recessive mutant in which the cell lineages are neotenic, reiterating L2 divisions, but the seam cells cease division and form adult alae precociously (during the late third larval stage). Thus, it appears that lin-14 may have at least three activities that independently control specific cell fates within given lineages: whether L1 or L2 division patterns occur in the first larval stage; whether L2 or L3 division patterns occur during the second stage; and whether adult alae are formed late during the third or fourth stage. In temperature-sensitive recessive mutants, the ts periods for determining which division pattern is generated by each of the blast cells in the first and second stage are short intervals just prior to the division of each cell. However, the ts period for the timing of adult alae formation is during the first larval stage, at least two cell divisions before that characteristic is expressed. New Heterochronic Genes. Based upon the phenotypic characteristics of lin-14 alleles (e.g. abnormal vulvae, lack of lateral alae), new heterochronic mutants were sought by examining egg-laying defective strains isolated in our laboratory. Four new mutants have been identified. There are three alleles of lin(n333) II. These neotenic mutants undergo supernumerary molts and seem to reiterate cell division patterns normally specific for the L3. Vulval morphogenesis is abnormal, and seam cells never form adult alae. The one allele of lin(n719) I was isolated by Chip Ferguson. This recessive mutant has the same precocious phenotype as the lin-14 mutants that delete L2- specific cell divisions. The n719 mutation suppresses lin-14 and lin- 4 neotenic mutants and can enhance lin-14 precocious mutants. This mutation may define a gene that interacts with lin-4 and lin-14 in controlling the temporal pattern of expression of specific cell fates. Dauer Recovery Suppresses Some Heterochronic Mutations. During routine handling of heterochronic mutant strains, we have noticed that dauer larvae from genotypically mutant strains often recover to become phenotypically normal, i.e. normal in the timing of vulval morphogenesis and of adult alae formation, as well as, in the case of certain neotenic strains, in the number of larval molts. Such phenotypic rescue occurs for both neotenic and precocious mutants of lin-14 and for lin(n719) I and has allowed us to mate strains otherwise too severely abnormal in vulval development. This phenomenon suggests that there exists a system that controls the timing of developmental events during dauer recovery and that this system can bypass the heterochrony induced by the mutations we have defined so far.