Tshz1 is required for axial skeleton, soft palate and middle ear development in mice

被引:49
作者
Core, Nathalie [1 ]
Caubit, Xavier
Metchat, Aiecha
Boned, Annie
Djabali, Malek
Fasano, Laurent
机构
[1] Univ Mediterranee, CNRS, UMR6216, IBDML, F-13288 Marseille 09, France
[2] CNRS, INSERM, Ctr Immuno Marseille Luminy, UMR6102,U631, F-13288 Marseille 09, France
关键词
Tshz1; mouse development; gene inactivation; middle ear; malleus; axial skeleton patterning; soft palate; CAA;
D O I
10.1016/j.ydbio.2007.05.038
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
Members of the Tshz gene family encode putative zinc fingers transcription factors that are broadly expressed during mouse embryogenesis. Tshz1 is detected from E9.5 in the somites, the spinal cord, the limb buds and the branchial arches. In order to assess the function of Tshzl during mouse development, we generated Tslizl-deficient mice. Tshzl inactivation leads to neonatal lethality and causes multiple developmental defects. In the craniofacial region, loss of Tshzl function leads to specific malformations of middle ear components, including the malleus and the tympanic ring. Tvhzl(-/-) mice exhibited Hox-like vertebral malformations and homeotic transformations in the cervical and thoracic regions, suggesting that Tshzl and Hox genes are involved in common pathways to control skeletal morphogenesis. Finally, we demonstrate that Tshzl is required for the development of the soft palate. (c) 2007 Elsevier Inc. All rights reserved.
引用
收藏
页码:407 / 420
页数:14
相关论文
共 69 条
  • [1] The Drosophila teashirt homeotic protein is a DNA-binding protein and modulo, a HOM-C regulated modifier of variegation, is a likely candidate for being a direct target gene
    Alexandre, E
    Graba, Y
    Fasano, L
    Gallet, A
    Perrin, L
    DeZulueta, P
    Pradel, J
    Kerridge, S
    Jacq, B
    [J]. MECHANISMS OF DEVELOPMENT, 1996, 59 (02) : 191 - 204
  • [2] Early postnatal lethality in Hoxa-5 mutant mice is attributable to respiratory tract defects
    Aubin, J
    Lemieux, M
    Tremblay, M
    Bérard, J
    Jeannotte, L
    [J]. DEVELOPMENTAL BIOLOGY, 1997, 192 (02) : 432 - 445
  • [3] Genetically altered mice: phenotypes, no phenotypes, and Faux phenotypes
    Barthold, SW
    [J]. GENETICA, 2004, 122 (01) : 75 - 88
  • [4] Bel S, 1998, DEVELOPMENT, V125, P3543
  • [5] Altered retinoic acid sensitivity and temporal expression of Hox genes in Polycomb-M33-deficient mice
    Bel-Vialar, S
    Coré, N
    Terranova, R
    Goudot, V
    Boned, A
    Djabali, M
    [J]. DEVELOPMENTAL BIOLOGY, 2000, 224 (02) : 238 - 249
  • [6] Combinatorial control of Drosophila eye development by eyeless, homothorax, and teashirt
    Bessa, J
    Gebelein, B
    Pichaud, F
    Casares, F
    Mann, RS
    [J]. GENES & DEVELOPMENT, 2002, 16 (18) : 2415 - 2427
  • [7] Haploinsufficiency of Sox9 results in defective cartilage primordia and premature skeletal mineralization
    Bi, WM
    Huang, WD
    Whitworth, DJ
    Deng, JM
    Zhang, ZP
    Behringer, RR
    de Crombrugghe, B
    [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2001, 98 (12) : 6698 - 6703
  • [8] Targeted disruption of hoxc-4 causes esophageal defects and vertebral transformations
    Boulet, AM
    Capecchi, MR
    [J]. DEVELOPMENTAL BIOLOGY, 1996, 177 (01) : 232 - 249
  • [9] Expression patterns of the three Teashirt-related genes define specific boundaries in the developing and postnatal mouse forebrain
    Caubit, X
    Tiveron, MC
    Cremer, H
    Fasano, L
    [J]. JOURNAL OF COMPARATIVE NEUROLOGY, 2005, 486 (01) : 76 - 88
  • [10] Vertebrate orthologues of the Drosophila region-specific patterning gene teashirt
    Caubit, X
    Coré, N
    Boned, A
    Kerridge, S
    Djabali, M
    Fasano, L
    [J]. MECHANISMS OF DEVELOPMENT, 2000, 91 (1-2) : 445 - 448