In silico-initiated cloning and molecular characterization of a novel human member of the L1 gene family of neural cell adhesion molecules |
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Authors: | Ming-Hui Wei Irina Karavanova Sergey V Ivanov Nicolae C Popescu Catherine L Keck Svetlana Pack Jonathan A Eisen M I Lerman |
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Institution: | (1) Intramural Research Support Program, SAIC Frederick, National Cancer Institute-Frederick Cancer Research and Development Center, Frederick, MD 21702-1201, USA, US;(2) Laboratory of Experimental Carcinogenesis, Molecular Cytogenetics Section, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA, US;(3) Laboratory of Pathology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA, US;(4) Department of Biological Sciences, Stanford University, Stanford, CA 94305–5020, USA, US;(5) Laboratory of Immunobiology, National Cancer Institute–Frederick Cancer Research and Development Center, Frederick, MD 21702-1201, USA e-mail: lerman@mail.ncifcrf.gov, Tel.: +1-301-8461288, Fax: +1-301-8466145, US |
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Abstract: | To discover genes contributing to mental retardation in 3p- syndrome patients we have used in silico searches for neural genes in NCBI databases (dbEST and UniGene). An EST with strong homology to the rat CAM L1 gene subsequently
mapped to 3p26 was used to isolate a full-length cDNA. Molecular analysis of this cDNA, referred to as CALL (cell adhesion L1-like), showed that it is encoded by a chromosome 3p26 locus and is a novel member of the L1 gene family of neural cell adhesion
molecules. Multiple lines of evidence suggest CALL is likely the human ortholog of the murine gene CHL1: it is 84% identical
on the protein level, has the same domain structure, same membrane topology, and a similar expression pattern. The orthology
of CALL and CHL1 was confirmed by phylogenetic analysis. By in situ hybridization, CALL is shown to be expressed regionally
in a timely fashion in the central nervous system, spinal cord, and peripheral nervous system during rat development. Northern
analysis and EST representation reveal that it is expressed in the brain and also outside the nervous system in some adult
human tissues and tumor cell lines. The cytoplasmic domain of CALL is conserved among other members of the L1 subfamily and
features sequence motifs that may involve CALL in signal transduction pathways.
Received: 14 April 1998 / Accepted: 18 June 1998 |
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