Results: DAB1 maps to chromosome 1 p31–p32, 2.53 cR centromeric from D1S417 and 6.4 cR distal from AFMA230VH5. Homologs: Human DAB1 is the ortholog of mouse Dab1, which maps to the cosyntenic region of mouse chromosome 4, in the vicinity of the Lepr locus (MGI:104993) (Fig.1). The Drosophila homolog is disabled. A second disabled-related gene, DAB2 (previously DOC-2), maps to human chromo- some 5p13, while its mouse ortholog, Dab2, has not yet been mapped (1). A related gene, M110.5, has been sequenced in Caenorhabditis elegans. As shown by Howell et al. (7), the greatest protein sequence conservation appears in an N- terminal region of 136 residues encompassing a putative phosphotyrosine binding domain. References 1. Albertsen, H. M., Smith, S. A., Melis, R., Williams, B., Holik, P., Stevens, J., and White, R. (1996). Sequence, genomic structure and chromosomal assignment of human DOC-2. Genomics 33: 207–213. 2. Chung, W. K., Power-Kehoe, L., Chua, M., and Leibel, R. L. (1996). Mapping of the OB receptor to 1p in a region of noncon- served gene order from mouse and rat to human. Genome Res. 6: 431– 438. 3. D’Arcangelo, G., Miao, G. G., Chen, S. C., Soares, H. D., Mor- gan, J. I., and Curran, T. (1995). A protein related to extracel- lular matrix proteins deleted in the mouse mutant reeler. Na- ture 374: 719 –723. 4. Gertler, F. B., Hill, K. K., Clark, M. J., and Hoffmann, F. M. (1993). Dosage-sensitive modifiers of Drosophila abl tyrosine kinase func- tion: prospero, a regulator of axonal growth, and disabled, a novel tyrosine kinase substrate. Genes Dev. 7: 441– 453. 5. Goldowitz, D., Cushing, R. C., Laywell, E., D’Arcangelo, G., Sheldon, M., Sweet, H. O., Davisson, M., Steindler, D., and Curran, T. (1997). Cerebellar disorganization characteristic of reeler in scrambler mutant mice despite presence of reelin. J. Neurosci. 17: 8767– 8777. 6. Gonzales, J. L., Russo, C. J., Goldowitz, D., Sweet, H. O., Davisson, M. T., and Walsh, C. A. (1997). Birthdate and cell marker analysis of scrambler: A novel mutation affecting cortical development with a reeler-like phenotype. J. Neurosci. 17: 9204 –9211. 7. Howell, B. W., Gertler, F. B., and Cooper, J. A. (1997). Mouse disabled (mDab1): a Src binding protein implicated in neuronal development. EMBO J. 16: 121–132. 8. Howell, B. W., Hawkes, R., Soriano, P., and Cooper, J. A. (1997). Neuronal position in the developing brain is regulated by mouse disabled-1. Nature 389: 733–737. 9. Lambert de Rouvroit, C., and Goffinet, A. M. (1988). The reeler mouse as a model of brain development. Adv. Anat. Embryol. Cell Biol. 150: 1–108. 10. Sheldon, M., Rice, D. S., D’Arcangelo, G., Yoneshima, H., Na- kajima, K., Mikoshiba, K., Howell, B., Cooper, J. A., Goldowitz, D., and Curran, T. (1997). Scrambler and yotari disrupt the disabled gene and produce a reeler-like phenotype on mice. Nature 389: 730 –733. 11. Ware, M. L., Fox, J. W., Davis, N. M., Lambert de Rouvroit, C., Russo, C., Chua, S. C., Jr., Goffinet, A. M., and Walsh, C. A. (1997). Aberrant splicing of a mouse disabled homolog, mDab1, in the scrambler mouse. Neuron 19: 239 –249. Assignment of Mouse Fibroblast Growth Factor 10 (Fgf10) Gene to the Telomeric Region of Chromosome 13 Michael A. Crackower,* , † Henry H. Q. Heng,† and Lap-Chee Tsui * , † ,1 * Department of Molecular and Medical Genetics, University of Toronto, Toronto, Ontario, Canada; and †Department of Genetics, The Hospital for Sick Children, Toronto, Ontario M5G 1X8, Canada Received July 6, 1998; accepted July 29, 1998 Functional gene description: Fibroblast growth factor 10 (Fgf10) has been shown to play an important role in verte- brate lung development (1) and limb morphogenesis (5). During early limb bud outgrowth, Fgf10 is expressed in the mesenchy- mal cells in the distal limb bud. Ectopic expression of Fgf10 showed that it was able to induce and maintain an ectopic apical ectodermal ridge (AER) (5). Thus it has been proposed that an endogenous role for Fgf10 may be to induce and main- tain the AER. Recently, human Fgf10 was mapped by radioac- tive in situ hybridization to chromosome 5p12–p13 (2). Name of clone or DNA source: The clones used were mouse Fgf10 partial cDNA obtained from Dr. Bridgid Hogan (1). Five positive PAC clones (RPCI21 365J17, 471H20, 530J2, 538D11, and 644L10) (Roswell Park) were isolated with the mouse Fgf10 cDNA by high-stringency hybridiza- tion screening of the gridded genomic library. Flanking markers used: A list of the markers was ob- tained electronically from The Jackson Laboratory home page at http://www.jax.org/resources/documents/cmdata. Methods of mapping: The chromosomal location of mouse Fgf10 was determined using FISH and genetic back- cross mapping. PAC clone (RPCI21 471H20) was biotinylated with dATP using the BRL Bionick labeling kit and used in FISH analysis following standard procedures (3). The chro- mosomal location of mouse Fgf10 was also investigated by interspecific backcross analysis using a panel of progeny DNA derived from matings of [(C57BL/6J  Mus spretus)F 1  C57BL/6J] mice (6). To detect informative RFLPs for this panel, C57BL/6J and M. spretus genomic DNA was digested with several restriction enzymes and analyzed by Southern blot with the mouse Fgf10 cDNA as probe. We thank Jack Huzienga for technical assistance, and Dr. Brigid Hogan for use of the fgf10 cDNA probe. We are grateful to Lucy Rowe and Mary Barter for their assistance with the backcross experi- ments. This work is supported by grants from the Canadian Genetic Disease Network and the Howard Hughes Medical Institute (Inter- national Scholar Program) to L.-C.T. M.A.C. is supported by an MRC (Canada) studentship. L.-C.T. is an MRC (Canada) Senior Scientist. 1 To whom correspondence should be addressed at Department of Genetics, The Hospital for Sick Children, 555 University Avenue, Toronto, Ontario M5G 1X8, Canada. Telephone: (416) 813-6015. Fax: (416) 813-4931. E-mail: lctsui@genet.sickkids.on.ca. 247 BRIEF MAPPING REPORTS GENOMICS 53, 247–248 (1998) ARTICLE NO. GE985506 0888-7543/98 $25.00 Copyright © 1998 by Academic Press All rights of reproduction in any form reserved.