<i>Small eyes</i>—a new dominant eye mutant in the mouse

Roberts, R. C.

doi:10.1017/s0016672300010387

Cited by 75 publications

(50 citation statements)

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“…Pax6 and Emx2 mutant embryos were obtained by intercrossing mice heterozygous for the Small eye mutant, Sey allele (Roberts, 1967;Hogan et al, 1986) and heterozygous Emx2ϩ/Ϫ mutants, respectively (Pellegrini et al, 1996), which were genotyped before use. All procedures followed Institute Animal Ethics Committee guidelines and National Institutes of Health guidelines for the care and use of animals.…”

Section: Methodsmentioning

confidence: 99%

Selective Requirement of Pax6, But Not Emx2, in the Specification and Development of Several Nuclei of the Amygdaloid Complex

Tole¹,

Remedios²,

Saha³

et al. 2005

J. Neurosci.

178

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The amygdaloid complex is a group of nuclei that are thought to originate from multiple sites of the dorsal and ventral telencephalic neuroepithelium. The mechanisms that regulate their development are essentially unknown. We studied the role of Pax6 and Emx2, two transcription factors that regulate regional specification and growth of the telencephalon, in the morphogenesis of the amygdaloid complex. We used a set of specific marker genes that identify distinct amygdaloid nuclei to analyze Pax6/Small eye and Emx2 knock-out mutant mouse brains. We found that there is a selective requirement for Pax6, but not Emx2, in the formation a subset of nuclei within the amygdaloid complex. Specifically, structures that were not previously considered to be developmentally linked, the nucleus of the lateral olfactory tract and the lateral, basolateral, and basomedial nuclei, all appear to have a common requirement for Pax6. Together, our findings provide new insights into the origins and mechanisms underlying the development of the amygdaloid complex.

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Section: Methodsmentioning

confidence: 99%

Selective Requirement of Pax6, But Not Emx2, in the Specification and Development of Several Nuclei of the Amygdaloid Complex

Tole¹,

Remedios²,

Saha³

et al. 2005

J. Neurosci.

178

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show abstract

“…These defects are shared with the small eye (Pax6 ϩ/Ϫ ) mouse, a model of the human syndromes (10)(11)(12). The small eye mouse model will aid in understanding the etiology of PAX6-associated disease and, in addition, provide insights into other anteriorsegment abnormalities.…”

Section: Ax6 Is Expressed In the Developing Lens Inner And Pigmentedmentioning

confidence: 99%

Primary defects in the lens underlie complex anterior segment abnormalities of thePax6heterozygous eye

Collinson

Quinn

Buchanan

et al. 2001

Proc. Natl. Acad. Sci. U.S.A.

114

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We describe lens defects in heterozygous small eye mice, and autonomous deficiencies of Pax6 ؉/؊ cells in the developing lens of Pax6 ؉/؉ 7 Pax6 ؉/؊ chimeras. Two separate defects of the lens were identified by analyzing the distribution of heterozygous cells in chimeras: Pax6 ؉/؊ cells are less readily incorporated into the lens placode than wild type, and those that are incorporated into the lens are not maintained efficiently in the proliferating lens epithelium. The lens of chimeric eyes is, therefore, predominantly wild type from embryonic day 16.5 onwards, whereas heterozygous cells contribute normally to all other eye tissues. Eye size and defects of the iris and cornea are corrected in fetal and adult chimeras with up to 80% mutant cells. Therefore, these aspects of the phenotype may be secondary consequences of primary defects in the lens, which has clinical relevance for the human aniridia (PAX6 ؉/؊ ) phenotype.

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“…Sey N~u arose on a (C3Hxl02)F 1 genetic background and was crossed to a CBA/Ca genetic background. The Sey allele (Roberts 1967) was maintained on a partially congenic CBA/Ca-Sey/+ stock. Other stocks were produced and maintained in the Centre for Reproductive Biology (Edinburgh).…”

Section: Micementioning

confidence: 99%

Multiple functions for Pax6 in mouse eye and nasal development.

Quinn¹,

West²,

Hill³

1996

Genes Dev.

221

156

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Mouse embryos, homozygous for the small eye (Sey) mutation die soon after birth with severe facial abnormalities that result from the failure of the eyes and nasal cavities to develop. Mutations in the Pax6 gene are responsible for the Sey phenotype. As a general disruption of eye and nasal development occurs in the homozygous Sey embryos, it is unclear, from the mutant phenotype alone, which tissues require functional Pax6. To examine the roles for Pax6 in eye and nasal development we produced chimeric mouse embryos composed of wild-type and Sey mutant cells. In these embryos we found that mutant cells were excluded from both the lens and nasal epithelium. Both of these tissues were smaller, and in some cases absent, in chimeras with high proportions of mutant cells. The morphology of the optic cup was also severely affected in these chimeras; mutant cells were excluded from the retinal pigmented epithelium and did not intermix with wild-type cells in other regions. The evidence shows that Pax6 has distinct roles in the nasal epithelium and the principal tissue components of the embryonic eye, acting directly and cell autonomously in the optic cup and lens. We suggest that Pax6 may promote cell surface changes in the optic cup and control the fate of the ectoderm from which the lens and nasal epithelia are derived.

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Small eyes—a new dominant eye mutant in the mouse

Abstract: A new mutant, Small eyes (symbol Sey), that reduces the size of the eye in the mouse, is described. It is dominant, and lethal when homozygous.

Cited by 75 publications

References 0 publications

Selective Requirement of Pax6, But Not Emx2, in the Specification and Development of Several Nuclei of the Amygdaloid Complex

Selective Requirement of Pax6, But Not Emx2, in the Specification and Development of Several Nuclei of the Amygdaloid Complex

Primary defects in the lens underlie complex anterior segment abnormalities of thePax6heterozygous eye

Multiple functions for Pax6 in mouse eye and nasal development.

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