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Resources » Paper

Rand JB et al. (1997) International C. elegans Meeting "ANALYSIS OF C. elegans CHOLINE ACETYLTRANSFERASE (CHA-1) MISSENSE MUTANTS SUGGESTS A TEMPERATURE-DEPENDENT REQUIREMENT FOR CHOLINERGIC FUNCTION"

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  • Comments on Rand JB et al. (1997) International C. elegans Meeting "ANALYSIS OF C. elegans CHOLINE ACETYLTRANSFERASE (CHA-1) MISSENSE MUTANTS SUGGESTS A TEMPERATURE-DEPENDENT REQUIREMENT FOR CHOLINERGIC FUNCTION" (0)

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    Status:
    Publication type:
    Meeting_abstract
    WormBase ID:
    WBPaper00022648

    Rand JB, Duerr JS, McManus JR, & Crowell T (1997). ANALYSIS OF C. elegans CHOLINE ACETYLTRANSFERASE (CHA-1) MISSENSE MUTANTS SUGGESTS A TEMPERATURE-DEPENDENT REQUIREMENT FOR CHOLINERGIC FUNCTION presented in International C. elegans Meeting. Unpublished information; cite only with author permission.

    The cha-1 and unc-17 genes encode choline acetyltransferase and a vesicular acetylcholine transporter respectively. Both of these genes are required for cholinergic transmission; and null alleles of both genes lead to L1 arrest and death. In addition, many viable cha-1 and unc-17 mutants have been isolated that have low levels of residual function. These mutants are small, slow-growing, uncoordinated, and resistant to inhibitors of cholinesterase. Some of the cha-1 mutants were reported to be temperature-sensitive, i.e., they were behaviorally normal at 16! but uncoordinated at 25!, or else the mutant phenotype was considerably stronger at the higher temperature. We sequenced and performed quantitative behavioral analysis on 16 viable cha-1 mutants with some residual gene function and thus some residual ChAT activity. Most of these mutations result in dramatic decreases in ChAT immunoreactivity in neurons, suggesting that the mutant proteins are preferentially degraded. In addition, most of these mutations confer temperature-sensitive development and behavior. While a few of the alleles have dramatic temperature effects, most cha-1 alleles tested exhibited at least mild heat-sensitivity of growth and behavior. (One allele showed both cold sensitivity and heat sensitivity; this mutation is due to a Tc1 insertion at a splice junction.) In contrast, neither unc-17 mutants nor snt-1 mutants displayed ts-growth or behavior. It thus appears that the requirement for acetylcholine itself may be temperature sensitive. (Supported by grants from NIGMS and OCAST.)

    Affiliation:
    - Oklahoma Medical Research Foundation, Oklahoma City, OK


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