Mutations at the fit1 locus affect normal pre- and post-natal development by retarding growth and reducing viability. We report mapping of the fit1 locus, by trans-complementation crosses to mice carrying deletions of the albino (c) locus in Chromosome (Chr) 7, to a subregion of the c-deletion complex within the Mod2-sh1 interval. The fit1 locus, which is currently defined by five N-ethyl-N-nitrosourea (ENU)-induced mutations, was found to map in a subregion between the eed and exed loci. A restriction fragment containing a deletion breakpoint that genetically defines the proximal border of fit1 was cloned, providing a DNA probe (RN302) that maps proximal to fit1. Long-range mapping with this probe, and with a DNA probe that maps distal to the fit1 interval, established that the region containing at least part of the fit1 gene is 530 kb or less. Positioning of fit1 between deletion breakpoints, and the isolation and mapping of a DNA probe proximal to it, should facilitate the cloning and molecular characterization of fit1, as well as of the eed locus and the tightly linked l(7)5Rn and l(7)6Rn loci.
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PLoS One
February 2013
Division of Pediatric Hematology-Oncology, Duke University Medical Center, Durham, North Carolina, USA.
The ubiquitously expressed phosphatidylinositol binding clathrin assembly (PICALM) protein associates with the plasma membrane, binds clathrin, and plays a role in clathrin-mediated endocytosis. Alterations of the human PICALM gene are present in aggressive hematopoietic malignancies, and genome-wide association studies have recently linked the PICALM locus to late-onset Alzheimer's disease. Inactivating and hypomorphic Picalm mutations in mice cause different degrees of severity of anemia, abnormal iron metabolism, growth retardation and shortened lifespan.
View Article and Find Full Text PDFGene
April 2012
College of Animal Science and Technology, Yangzhou University, Yangzhou, China.
Escherichia coli (E. coli) that produces adhesin F18 is the main pathogen responsible for porcine post-weaning diarrhea and edema disease. The receptor for E.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
July 2003
Department of Biochemistry and Cellular and Molecular Biology, University of Tennessee, Knoxville, TN 37996, USA.
Recessive N-ethyl-N-nitrosourea (ENU)-induced mutations recovered at the fitness-1 (fit1) locus in mouse chromosome 7 cause hematopoietic abnormalities, growth retardation, and shortened life span, with varying severity of the defects in different alleles. Abnormal iron distribution and metabolism and frequent scoliosis have also been associated with an allele of intermediate severity (fit14R). We report that fit14R, as well as the most severe fit15R allele, are nonsense point mutations in the mouse ortholog of the human phosphatidylinositol-binding clathrin assembly protein (PICALM) gene, whose product is involved in clathrin-mediated endocytosis.
View Article and Find Full Text PDFJ Gen Virol
April 2002
Leukemogenesis Section, Laboratory of Cellular Oncology, National Cancer Institute, NIH, Bethesda, MD 20892-4255, USA1.
Mml loci have been identified as provirus integration sites among a subset of monocytic tumours induced by murine leukaemia virus (MuLV) infection of BALB/c and DBA/2 mice. These myeloid leukaemias contain a retrovirus integrated on chromosome 10 in proximity to the c-myb locus; however, c-myb expression was not altered. Detailed physical mapping enabled placement of the retroviral integration sites approximately 25 kb (Mml1), approximately 51 kb (Mml2), and approximately 70 kb (Mml3) upstream of the c-myb locus.
View Article and Find Full Text PDFLab Anim Sci
June 1999
Department of Pathology, The University of Tennessee, Knoxville 37901-1071, USA.
Background And Purpose: Previous investigation of fitness1(4226SB) mice revealed growth retardation and microcytic, hypochromic anemia with functional iron deficiency. Serum biochemical analysis suggested protein-losing enteropathy and liver dysfunction.
Methods: Radiography was done to assess lumbar bone lesions in mice hemizygous for fitness1 (fit1) [c fit1(4226SB/Df(c Mod2 sh1)26DVT] and age-matched sibling controls [c(ch)+/c(ch)+] at 40 or 60 days of age.
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