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Resources » Paper

Daigle I et al. (1995) International C. elegans Meeting "Characterization of apl-1, an amyloid precursor-related gene from Caenorhabditis elegans."

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  • Comments on Daigle I et al. (1995) International C. elegans Meeting "Characterization of apl-1, an amyloid precursor-related gene from Caenorhabditis elegans." (0)

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    Status:
    Publication type:
    Meeting_abstract
    WormBase ID:
    WBPaper00021720

    Daigle I, & Li C (1995). Characterization of apl-1, an amyloid precursor-related gene from Caenorhabditis elegans presented in International C. elegans Meeting. Unpublished information; cite only with author permission.

    Alzheimer's disease is a neurodegenerative disease for which the cause is still unknown. Accumulation of a b-amyloid peptide in the brain of patients has been associated with the disease; the normal function and processing of the amyloid protein precursor (APP), from which the b-peptide is derived, remain to be understood. A family of APP-related proteins have been identified and appear to be conserved through evolution. We are interested in possibly elucidating a function of APP by looking at APP-related genes in Caenorhabditis elegans. We have isolated and characterized APP-related cDNAs from C. elegans, and called the corresponding gene apl-1. The putative translation product, APL-1, is a new member of the APP family of proteins. apl-1 transcripts do not appear to be alternatively spliced, but differ in the length of their 3' untranslated region. They are trans-spliced to an SL1 leader sequence. The genomic region corresponding to apl-1 spans about 4 kbp and contains 12 exons and 11 introns. It has been positioned to the left arm of the X chromosome of C. elegans. Only one apl-like gene appears to be present in C. elegans. To examine the cell-specific transcription of apl-1, transgenic animals carrying different regions of the apl-1 promotor are being produced. To examine the function of apl-1, we have obtained a mutant strain containing a Tc1 transposon inserted in apl-1 (kindly provided by Dr. Ronald Plasterk). The Tc1 insertion site has been located to exon 12, one codon after the beginning of the putative transmembrane domain coding sequence. Characterization of the insertion mutant, together with a screen for excision mutants, is underway. Transgenic worms overexpressing apl-1 are being constructed.


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