SgIGSF: a new mast-cell adhesion molecule used for attachment to fibroblasts and transcriptionally regulated by MITF.

Microphthalmia transcription factor (MITF) is a basic-helix-loop-helix-leucine zipper-type transcription factor. The mutant mi and Mi(wh) alleles encode MITFs with deletion and alteration of a single amino acid, respectively, whereas the tg is a null mutation. In coculture with NIH/3T3 fibroblasts, the numbers of cultured mast cells (CMCs) derived from C57BL/6 (B6)(mi/mi), B6(Miwh/Miwh), and B6(tg/tg) mice that adhered to NIH/3T3 fibroblasts were one third as large as the number of B6(+/+) CMCs that adhered to NIH/3T3 fibroblasts. From a cDNA library of B6(+/+) CMCs, we subtracted messenger RNAs expressed by B6(mi/mi) CMCs and found a clone encoding SgIGSF, a recently identified member of the immunoglobulin superfamily. Northern and Western blot analyses revealed that SgIGSF was expressed in B6(+/+) CMCs but not in CMCs derived from MITF mutants. Immunocytochemical analysis showed that SgIGSF localized to the cell-to-cell contact areas between B6(+/+) CMCs and NIH/3T3 fibroblasts. Transfection of B6(mi/mi) and B6(tg/tg) CMCs with SgIGSF cDNA normalized their adhesion to NIH/3T3 fibroblasts. NIH/3T3 fibroblasts did not express SgIGSF, indicating that SgIGSF acts as a heterophilic adhesion molecule. Transfection of B6(tg/tg) CMCs with normal MITF cDNA elevated their SgIGSF expression to normal levels. These results indicated that SgIGSF mediated the adhesion of CMCs to fibroblasts and that the transcription of SgIGSF was critically regulated by MITF.

[1]  E. Morii,et al.  Dual abnormal effects of mutant MITF encoded by Mi(wh) allele on mouse mast cells: decreased but recognizable transactivation and inhibition of transactivation. , 2002, Biochemical and biophysical research communications.

[2]  H. Fukuhara,et al.  The Tumor Suppressor Protein TSLC1 Is Involved in Cell-Cell Adhesion* , 2002, The Journal of Biological Chemistry.

[3]  N. Copeland,et al.  Mitf and Tfe3, two members of the Mitf-Tfe family of bHLH-Zip transcription factors, have important but functionally redundant roles in osteoclast development , 2002, Proceedings of the National Academy of Sciences of the United States of America.

[4]  K. Tamura,et al.  Use of stepwise subtraction to comprehensively isolate mouse genes whose transcription is up‐regulated during spermiogenesis , 2002, EMBO reports.

[5]  E. Morii,et al.  Interaction and Cooperation of mi Transcription Factor (MITF) and Myc-associated Zinc-finger Protein-related Factor (MAZR) for Transcription of Mouse Mast Cell Protease 6 Gene* , 2002, The Journal of Biological Chemistry.

[6]  E. Morii,et al.  Isoforms of mi transcription factor preferentially expressed in cultured mast cells of mice. , 2002, Biochemical and biophysical research communications.

[7]  K. Ohashi,et al.  Cloning and characterization of a novel mouse immunoglobulin superfamily gene expressed in early spermatogenic cells , 2001, Molecular reproduction and development.

[8]  H. Fukuhara,et al.  Isolation of the TSLL1 and TSLL2 genes, members of the tumor suppressor TSLC1 gene family encoding transmembrane proteins , 2001, Oncogene.

[9]  H. Fukuhara,et al.  Identification of tumor suppressor candidate genes by physical and sequence mapping of the TSLC1 region of human chromosome 11q23. , 2001, Gene.

[10]  H. Handa,et al.  Inhibitory effect of the mi transcription factor encoded by the mutant mi allele on GA binding protein-mediated transcript expression in mouse mast cells. , 2001, Blood.

[11]  H. Fukuhara,et al.  TSLC1 is a tumor-suppressor gene in human non-small-cell lung cancer , 2001, Nature Genetics.

[12]  Y. Kitamura,et al.  Independent influence of strain difference and mi transcription factor on the expression of mouse mast cell chymases. , 2001, The American journal of pathology.

[13]  H. Hanafusa,et al.  v-Crk activates the phosphoinositide 3-kinase/AKT pathway in transformation. , 2000, Proceedings of the National Academy of Sciences of the United States of America.

[14]  H Nojima,et al.  A truncated isoform of the PP2A B56 subunit promotes cell motility through paxillin phosphorylation , 2000, The EMBO journal.

[15]  K. Tachibana,et al.  Interaction of Nectin with Afadin Is Necessary for Its Clustering at Cell-Cell Contact Sites but Not for Itscis Dimerization or trans Interaction* , 2000, The Journal of Biological Chemistry.

[16]  M. Hattori,et al.  A 2-Mb sequence-ready contig map and a novel immunoglobulin superfamily gene IGSF4 in the LOH region of chromosome 11q23.2. , 1999, Genomics.

[17]  E. Morii,et al.  Different effect of various mutant MITF encoded by mi, Mior, or Miwh allele on phenotype of murine mast cells. , 1999, Blood.

[18]  A. Nomoto,et al.  Nectin/PRR: An Immunoglobulin-like Cell Adhesion Molecule Recruited to Cadherin-based Adherens Junctions through Interaction with Afadin, a PDZ Domain–containing Protein , 1999, The Journal of cell biology.

[19]  E. Morii,et al.  Deficient transcription of mouse mast cell protease 4 gene in mutant mice of mi/mi genotype. , 1999, Blood.

[20]  E. Morii,et al.  Inhibitory effect of the transcription factor encoded by the mi mutant allele in cultured mast cells of mice. , 1999, Blood.

[21]  E. Morii,et al.  Systematic method to obtain novel genes that are regulated by mi transcription factor: impaired expression of granzyme B and tryptophan hydroxylase in mi/mi cultured mast cells. , 1998, Blood.

[22]  E. Morii,et al.  Abnormal expression of mouse mast cell protease 5 gene in cultured mast cells derived from mutant mi/mi mice. , 1997, Blood.

[23]  T. Kondo,et al.  Involvement of transcription factor encoded by the mouse mi locus (MITF) in apoptosis of cultured mast cells induced by removal of interleukin-3. , 1997, The American journal of pathology.

[24]  J. Davoust,et al.  Selective control of membrane ruffling and actin plaque assembly by the Rho GTPases Rac1 and CDC42 in FcepsilonRI-activated rat basophilic leukemia (RBL-2H3) cells. , 1997, Journal of cell science.

[25]  鈴木 公子.  The Recessive Phenotype Displayed by a Dominant Negative Microphthalmiat-Associated Transcription Factor Mutant Is a Result of Impaired Nuclear Localization Potential. , 1997 .

[26]  E. Morii,et al.  Regulation of mouse mast cell protease 6 gene expression by transcription factor encoded by the mi locus. , 1996, Blood.

[27]  T. Kondo,et al.  Involvement of transcription factor encoded by the mi locus in the expression of c-kit receptor tyrosine kinase in cultured mast cells of mice. , 1996, Blood.

[28]  E. Morii,et al.  The recessive phenotype displayed by a dominant negative microphthalmia-associated transcription factor mutant is a result of impaired nucleation potential , 1996, Molecular and cellular biology.

[29]  E. Morii,et al.  Loss of DNA binding ability of the transcription factor encoded by the mutant mi locus. , 1994, Biochemical and biophysical research communications.

[30]  James A. Vaught,et al.  microphthalmia, a critical factor in melanocyte development, defines a discrete transcription factor family. , 1994, Genes & development.

[31]  A. Ferré-D’Amaré,et al.  Molecular basis of mouse microphthalmia (mi) mutations helps explain their developmental and phenotypic consequences , 1994, Nature Genetics.

[32]  M. Morimoto,et al.  Deficient differentiation of mast cells in the skin of mi/mi mice. Usefulness of in situ hybridization for evaluation of mast cell phenotype. , 1993, The American journal of pathology.

[33]  J. Lingrel,et al.  A helix-loop-helix transcription factor-like gene is located at the mi locus. , 1993, The Journal of biological chemistry.

[34]  N. Jenkins,et al.  Mutations at the mouse microphthalmia locus are associated with defects in a gene encoding a novel basic-helix-loop-helix-zipper protein , 1993, Cell.

[35]  J. Esko,et al.  Stable heparin-producing cell lines derived from the Furth murine mastocytoma. , 1992, Proceedings of the National Academy of Sciences of the United States of America.

[36]  J. Fex,et al.  Cochlear disorder associated with melanocyte anomaly in mice with a transgenic insertional mutation , 1992, Molecular and Cellular Neuroscience.

[37]  S. Nishikawa,et al.  Low c-kit expression of cultured mast cells of mi/mi genotype may be involved in their defective responses to fibroblasts that express the ligand for c-kit. , 1992, Blood.

[38]  S. Nishikawa,et al.  Necessity of extracellular domain of W (c-kit) receptors for attachment of murine cultured mast cells to fibroblasts. , 1992, Blood.

[39]  S. Nishikawa,et al.  Exon skipping by mutation of an authentic splice site of c-kit gene in W/W mouse. , 1991, Nucleic acids research.

[40]  S. Nagata,et al.  pEF-BOS, a powerful mammalian expression vector. , 1990, Nucleic acids research.

[41]  K. Nocka,et al.  Molecular bases of dominant negative and loss of function mutations at the murine c‐kit/white spotting locus: W37, Wv, W41 and W. , 1990, The EMBO journal.

[42]  Y. Kitamura,et al.  Failure of W/Wv mouse-derived cultured mast cells to enter S phase upon contact with NIH/3T3 fibroblasts , 1988 .

[43]  T. Honjo,et al.  Fibroblast‐dependent growth of mouse mast cells in vitro: Duplication of mast cell depletion in mutant mice of w/wv genotype , 1988, Journal of cellular physiology.

[44]  Makio,et al.  Clonal assay of mouse mast cell colonies in methylcellulose culture. , 1982, Blood.

[45]  C. Witkop.  The Coat Colors of Mice. A Model for Mammalian Gene Action and Interaction , 1980 .

[46]  W. Silvers.  The coat colours of mice. A model for mammalian gene action and interaction. , 1979 .

[47]  W. Silvers.  The Coat Colors of Mice , 1979, Springer New York.