The Opitz syndrome gene MID1 is essential for establishing asymmetric gene expression in Hensen's node

Developmental Biology

Volumn 258, Issue 2, 2003, Pages 397-405

  Granata, Alessandra ^a   Quaderi, Nandita A ^a  

^a GUY S HOSPITAL   (United Kingdom)

Author keywords

Antisense morpholinos; BMP4; Chick; Hensen's node; L R asymmetry; MID1; Opitz syndrome; SHH

Indexed keywords

ARTICLE; CHICKEN; EMBRYONIC STRUCTURES; GENE EXPRESSION; GENE INTERACTION; GENE REPRESSION; MODEL; NONHUMAN; NUCLEOTIDE SEQUENCE; OPITZ SYNDROME; PRIORITY JOURNAL; SIGNAL TRANSDUCTION;

AVES; GALLUS GALLUS;

EID: 0038545491     PISSN: 00121606     EISSN: None     Source Type: Journal    
DOI: 10.1016/S0012-1606(03)00131-3     Document Type: Article

References (32)

1. Belloni E., et al. Identification of Sonic hedgehog as a candidate gene responsible for holoprosencephaly. Nat. Genet. 14:1996;353-356.
2. Boettger T., et al. FGF8 functions in the specification of the right body side of the chick. Curr. Biol. 9:1999;277-280.
3. Buchner G., et al. MID2, a homologue of the Opitz syndrome gene MID1 similarities in subcellular localization and differences in expression during development . Hum. Mol. Genet. 8:1999;1397-1407.
4. Capdevila J., et al. Mechanisms of left-right determination in vertebrates. Cell. 101:2000;9-21.
5. Chapman S.C., et al. Improved method for chick whole-embryo culture using a filter paper carrier. Dev. Dyn. 220:2001;284-289.
6. Cox T.C., et al. New mutations in MID1 provide support for loss of function as the cause of X-linked Opitz syndrome. Hum. Mol. Genet. 9:2000;2553-2562.
7. Ericson J., et al. Two critical periods of Sonic Hedgehog signaling required for the specification of motor neuron identity. Cell. 87:1996;661-673.
8. Essner J.J., et al. Conserved function for embryonic nodal cilia. Nature. 418:2002;37-38.
9. Garcia-Castro M.I., et al. N-Cadherin, a cell adhesion molecule involved in establishment of embryonic left-right asymmetry. Science. 288:2000;1047-1051.
10. Gaudenz K., et al. Opitz G/BBB syndrome in Xp22 mutations in the MID1 gene cluster in the carboxy-terminal domain . Am. J. Hum. Genet. 63:1998;703-710.
11. Hahn H., et al. Mutations of the human homolog of Drosophila patched in the nevoid basal cell carcinoma syndrome. Cell. 85:1996;841-851.
12. Isaac A., et al. Control of vertebrate left-right asymmetry by a snail-related zinc finger gene. Science. 275:1997;1301-1304.
13. Johnson R.L., et al. Human homolog of patched, a candidate gene for the basal cell nevus syndrome. Science. 272:1996;1668-1671.
14. Kawakami M., Nakanishi N. The role of an endogenous PKA inhibitor, PKIalpha, in organizing left-right axis formation. Development. 128:2001;2509-2515.
15. Levin M., Mercola M. Gap junction-mediated transfer of left-right patterning signals in the early chick blastoderm is upstream of Shh asymmetry in the node. Development. 126:1999;4703-4714.
16. Levin M., et al. A molecular pathway determining left-right asymmetry in chick embryogenesis. Cell. 82:1995;803-814.
17. Levin M., et al. Left/right patterning signals and the independent regulation of different aspects of situs in the chick embryo. Dev. Biol. 189:1997;57-67.
18. Levin M., et al. Asymmetries in H(+)/K(+)-ATPase and cell membrane potentials comprise a very early step in left-right patterning. Cell. 111:2002;77.
19. Liu J., et al. Phosphorylation and microtubule association of the Opitz syndrome protein mid-1 is regulated by protein phosphatase 2A via binding to the regulatory subunit alpha 4. Proc. Natl. Acad. Sci. USA. 98:2001;6650-6655.
20. Meyers E.N., Martin G.R. Differences in left-right axis pathways in mouse and chick functions of FGF8 and SHH . Science. 285:1999;403-406.
21. Monsoro-Burq A., Le Douarin N.M. BMP4 plays a key role in left-right patterning in chick embryos by maintaining Sonic Hedgehog asymmetry. Mol. Cell. 7:2001;789-799.
22. Myat A., et al. A chick homologue of Serrate and its relationship with Notch and Delta homologues during central neurogenesis. Dev. Biol. 174:1996;233-247.
23. Pagan-Westphal S.M., Tabin C.J. The transfer of left-right positional information during chick embryogenesis. Cell. 93:1998;25-35.
24. Quaderi N.A., et al. Opitz G/BBB syndrome, a defect of midline development, is due to mutations in a new RING finger gene on Xp22. Nat. Genet. 17:1997;285-291.
25. Richman J.M., et al. Isolation and characterisation of the chick orthologue of the Opitz syndrome gene, Mid1, supports a conserved role in vertebrate development. Int. J. Dev. Biol. 46:2002;441-448.
26. Rodriguez-Esteban C., et al. Wnt signaling and PKA control Nodal expression and left-right determination in the chick embryo. Development. 128:2001;3189-3195.
27. Roessler E., et al. Mutations in the human Sonic Hedgehog gene cause holoprosencephaly. Nat. Genet. 14:1996;357-360.
28. Roessler E., Muenke M. Midline and laterality defects left and right meet in the middle . Bioessays. 23:2001;888-900.
29. Sontag E. Protein phosphatase 2A the Trojan Horse of cellular signaling . Cell Signal. 13:2001;7-16.
30. Trockenbacher A., et al. MID1, mutated in Opitz syndrome, encodes an ubiquitin ligase that targets phosphatase 2A for degradation. Nat. Genet. 29:2001;287-294.
31. Vortkamp A., et al. GLI3 zinc-finger gene interrupted by translocations in Greig syndrome families. Nature. 352:1991;539-540.
32. Wright C.V. Mechanisms of left-right asymmetry what's right and what's left? Dev. Cell. 1:2001;179-186.