“Bent-Tail,” A Dominant, Sex-Linked Mutation in the Mouse

Garber, E. D.

doi:10.1073/pnas.38.10.876

Cited by 47 publications

(19 citation statements)

References 3 publications

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“…These mice were kept in a C57BL/6J background. The spontaneous mutation in the Bent tail (Bn) (Garber, 1952) mouse has been revealed to be a deletion of the X chromosome, including Zic3 (Carrel et al, 2000;Klootwijk et al, 2000). The phenotypes of Bn mice are very similar to those of Zic3-deficient mice generated by targeted mutation (Purandare et al, 2002;Aruga et al, 2004).…”

Section: Methodsmentioning

confidence: 86%

Zic1andZic3Regulate Medial Forebrain Development through Expansion of Neuronal Progenitors

Inoue¹,

Ota²,

Ogawa³

et al. 2007

J. Neurosci.

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The medial telencephalon is a source of neurons that follow distinct tangential trajectories of migration to various structures such as the cerebral cortex, striatum, and olfactory bulb. In the present study, we characterized the forebrain anomalies in Zic1/Zic3 compound mutant mice. Zic1 and Zic3 were strongly expressed in the medial structures, including the septum, medial cerebral cortex, and choroid plexus. Mice homozygous for the Zic1 mutant allele together with the null Zic3 allele showed medial forebrain defects, which were not obvious in either Zic1 or Zic3 single mutants. Absence of both Zic1 and Zic3 caused hypoplasia of the hippocampus, septum, and olfactory bulb. Analysis of the cell cycle revealed that the cell cycle exit rate was increased in the septa of double mutants. Misexpression of Zic3 in the ventricular layer of the cerebral cortex inhibited neuronal differentiation. These results indicated that both Zic1 and Zic3 function in maintaining neural precursor cells in an undifferentiated state. The functions of these genes may be essential to increasing neural cell numbers regionally in the medial telencephalon and to proper mediolateral patterning of the telencephalon.

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Section: Methodsmentioning

confidence: 86%

Zic1andZic3Regulate Medial Forebrain Development through Expansion of Neuronal Progenitors

Inoue¹,

Ota²,

Ogawa³

et al. 2007

J. Neurosci.

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“…The spontaneous mutation Bn, which was first described by Garber (1952), originally occurred in an F1-male from a cross of a Namru strain female and a bald hr ba /hr ba male. The Bent tail mice in the current study were obtained from Jackson Laboratories (Bar Harbor, ME).…”

Section: Materials and Methods Bent Tail Mouse (Bn)mentioning

confidence: 99%

Phenotype of the neural tube defect mouse model bent tail is not sensitive to maternal folinic acid, myo‐inositol, or zinc supplementation

Franke¹,

Klootwijk²,

Lemmers³

et al. 2003

Birth Defects Research

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“…Part of the excluded chromosomal segment, i.e. the region overlapping the genes for HPRT, L1CAM and F8C, has syntenic homology with the region of the murine X chromosome (Lyon and Kirby 1992) encompassing the locus for "bent tail" (Bn), a mouse model for X-linked NTD (Garber 1952). Our resuits therefore indicate that the human homologue of the murine Bn gene is different from the gene underlying NTD in the present family.…”

Section: Discussionmentioning

confidence: 57%

Exclusion mapping of the gene for X-linked neural tube defects in an Icelandic family

et al. 1994

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Various polymorphic markers with a random distribution along the X chromosome were used in a linkage analysis performed on a family with apparently X-linked recessive inheritance of neural tube defects (NTD). The lod score values were used to generate an exclusion map of the X chromosome; this showed that the responsible gene was probably not located in the middle part of Xp or in the distal region of Xq. A further refining of these results was achieved by haplotype analysis, which indicated that the gene for X-linked NTD was located either within Xp21.1-pter, distal from the DMD locus, or in the region Xq12-q24 between DXS106 and DXS424. Multipoint linkage analysis revealed that the likelihood for gene location is highest for the region on Xp. The region Xq26-q28, which has syntenic homology with the segment of the murine X chromosome carrying the locus for 'bent tail' (Bn), a mouse model for X-linked NTD, is excluded as the location for the gene underlying X-linked NTD in the present family. Thus, the human homologue of the Bn gene and the present defective gene are not identical, suggesting that more than one gene on the X chromosome plays a role in the development of the neural tube.

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“Bent-Tail,” A Dominant, Sex-Linked Mutation in the Mouse

Cited by 47 publications

References 3 publications

Zic1andZic3Regulate Medial Forebrain Development through Expansion of Neuronal Progenitors

Zic1andZic3Regulate Medial Forebrain Development through Expansion of Neuronal Progenitors

Phenotype of the neural tube defect mouse model bent tail is not sensitive to maternal folinic acid, myo‐inositol, or zinc supplementation

Exclusion mapping of the gene for X-linked neural tube defects in an Icelandic family

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