Publications (3)15.34 Total impact

  • Holly Soehnge · Xi Huang · Marie Becker · Diana Conover · Michael Stern
    [Show abstract] [Hide abstract] ABSTRACT: Two closely linked genes were identified and characterized in the 24F region on the left arm of chromosome 2 in Drosophila. One cDNA predicts a protein of 231 amino acids, with a molecular mass of 25.7 kDa. The predicted amino-acid sequence of this protein is 47.2% identical to that of the previously reported human GS1 protein, which is encoded by a gene that is of interest because it is one of the few X-linked genes that escapes X-inactivation. We have accordingly named our gene GS1like (GS1l). The second cDNA begins 383 bp proximal to the first. This cDNA encodes a protein of a predicted 149 amino acids and a molecular mass of 17.0 kDa. This protein represents a homolog of ribosomal protein L27a; thus, we have named the gene RpL27a. This gene might be responsible for the Minute mutation located at 24F. An rpL27a gene was previously localized to 87F/88A; thus, this gene might be present in two locations in Drosophila.
    No preview · Article · Mar 1997 · Gene
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    H Soehnge · A Ouhtit · O N Ananthaswamy
    [Show abstract] [Hide abstract] ABSTRACT: Ultraviolet (UV) radiation is the carcinogenic factor in sunlight; damage to skin cells from repeated exposure can lead to the development of cancer. UV radiation has been mainly implicated as the cause of non-melanoma skin cancer, although some role for UV in malignant melanoma has been suggested. The induction of skin cancer is mainly caused by the accumulation of mutations caused by UV damage. Cellular mechanisms exist to repair the DNA damage, or to induce apoptosis to remove severely damaged cells; however, the additive effects of mutations in genes involved in these mechanisms, or in control of the cell cycle, can lead to abnormal cell proliferation and tumor development. The molecular events in the induction of skin cancer are being actively investigated, and recent research has added to the understanding of the roles of tumor suppressor and oncogenes in skin cancer. UV radiation has been shown to induce the expression of the p53 tumor suppressor gene, and is known to produce "signature" mutations in p53 in human and mouse skin cancers and in the tumor suppressor gene patched in human basal cell carcinoma. The role of UV radiation in suppression of immune surveillance in the skin, which is an important protection against skin tumor development, is also being investigated. The knowledge gained will help to better understand the ways in which skin cancer arises from UV exposure, which will in turn allow development of better methods of treatment and prevention.
    Full-text · Article · Feb 1997 · Frontiers in Bioscience
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    H Soehnge · X Huang · M Becker · P Whitley · D Conover · M Stern
    [Show abstract] [Hide abstract] ABSTRACT: Behavioral and electrophysiological studies on mutants defective in the Drosophila inebriated (ine) gene demonstrated increased excitability of the motor neuron. In this paper, we describe the cloning and sequence analysis of ine. Mutations in ine were localized on cloned DNA by restriction mapping and restriction fragment length polymorphism (RFLP) mapping of ine mutants. DNA from the ine region was then used to isolate an ine cDNA. In situ hybridization of ine transcripts to developing embryos revealed expression of this gene in several cell types, including the posterior hindgut, Malpighian tubules, anal plate, garland cells, and a subset of cells in the central nervous system. The ine cDNA contains an open reading frame of 658 amino acids with a high degree of sequence similarity to members of the Na+/Cl(-)-dependent neurotransmitter transporter family. Members of this family catalyze the rapid reuptake of neurotransmitters released into the synapse and thereby play key roles in controlling neuronal function. We conclude that ine mutations cause increased excitability of the Drosophila motor neuron by causing the defective reuptake of the substrate neurotransmitter of the ine transporter and thus overstimulation of the motor neuron by this neurotransmitter. From this observation comes a unique opportunity to perform a genetic dissection of the regulation of excitability of the Drosophila motor neuron.
    Full-text · Article · Dec 1996 · Proceedings of the National Academy of Sciences