BMP4 is essential for lens induction in the mouse embryo

Furuta, Yasuhide; Hogan, Brigid L.M.

doi:10.1101/gad.12.23.3764

Cited by 410 publications

(458 citation statements)

References 53 publications

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“…Pax6 is upstream of Sox2 (Furuta and Hogan, 1998), Pax6 and Sox2 cooperatively regulate gene expression (Kamachi et al 2001, Aota et al, 2003, and Sox2 is required for the maintenance of Pax6 (Donner et al, in press). Appropriate temporal, spatial, and quantitative control of Pax6 expression is required for appropriate lens morphogenesis (Hill et al, 1991;Glaser et al, 1994;Hanson et al, 1994;Grindley et al, 1995;Quinn et al, 1996;Schedl et al, 1996;Brown et al, 1998;Ashery-Padan et al, 2000;Duncan et al, 2000;van Raamsdonk and Tilgham, 2000;Dimanlig et al, 2001;Duncan et al, 2004).…”

Section: Resultsmentioning

confidence: 99%

Pax6 is misexpressed in Sox1 null lens fiber cells

Donner

Episkopou

et al. 2007

Gene Expression Patterns

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Sox1 null lens fiber cells fail to elongate and have disrupted expression of gamma crystallin. We have evaluated the expression of Sox1 and Pax6 proteins during critical stages of lens morphogenesis, with particular focus on fiber cell differentiation. While Pax6 and Sox1 are co-expressed during early stages of fiber cell differentiation, Sox1 up-regulation coincides temporally with the down-regulation of Pax6, and these proteins therefore display a striking inverse expression pattern in the lens fiber cell compartment. Furthermore, Pax6 is inappropriately expressed in the fiber cells of Sox1 null mice and the Pax6 target, α5 integrin, is simultaneously misexpressed. Finally, we demonstrate a genetic interaction between Sox1 and Pax6, as Sox1 heterozygosity partially rescues the diameter of Pax6 Sey lenses by increasing the number of cells in the fiber cell compartment.

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Section: Resultsmentioning

confidence: 99%

Pax6 is misexpressed in Sox1 null lens fiber cells

Donner

Episkopou

et al. 2007

Gene Expression Patterns

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“…16 It is upregulated in the presumptive lens ectoderm at E9.5 and continues to be expressed in the lens and neural retina in early eye development. 17 At E10.5 and E11.5, Sox2 expression is present at the optic fissure margins during optic fissure closure as shown in parasagittal sections (Figure 2d). …”

Section: Clinical Findingsmentioning

confidence: 99%

Novel SOX2 partner-factor domain mutation in a four-generation family

et al. 2009

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Anophthalmia (no eye), microphthalmia (small eye) and associated ocular developmental anomalies cause significant visual handicap. In most cases the underlying genetic cause is unknown, but mutations in some genes, such as SOX2, cause ocular developmental defects, particularly anophthalmia, in a subset of patients. Here, we describe a four-generation family with a p.Asp123Gly mutation in the highly conserved partner-factor interaction region of the SOX2 protein, which is important for cell-specific actions of SOX2. The proband in this family has bilateral anophthalmia and several other family members have milder ocular phenotypes, including typical optic fissure coloboma. Expression studies indicate that Sox2 is expressed in the eye at the site of closure of the optic fissure during development. The SOX2 mutation in this family implicates the partner-factor interaction region of SOX2 in contributing to the specificity of SOX2 action in optic fissure closure. Our findings indicate that investigation of SOX2 in a broad range of eye anomaly patients aids in the determination of particular functions of SOX2 in development.

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“…Embryos were collected from C57Bl mice at the appropriate developmental stage, fixed in paraformaldehyde, embedded in paraffin, sectioned and stained using previously described procedures. 13 …”

Section: Methodsmentioning

confidence: 99%

Developmental Expression of Two CXC Chemokines, Mip-2 and Kc, and Their Receptors

Luan

Furuta

et al. 2001

Cytokine

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CXC chemokines, macrophage inflammatory protein-2 (MIP-2) and KC, (a cloning designation based on ordinate and abscissa position) as well as the CXC chemokine receptor, CXCR2, are expressed in a variety of cells and tissues in adult mice. Targeted deletion of the gene encoding murine CXCR2 does not result in obvious changes in the development of the organ system of the mouse, though the CXCR2 −/− mouse is compromised with regard to its ability to resist infection, heal wounds, and maintain homeostasis when challenged with microbes and/or chemicals. In an attempt to develop insight into additional possible subtle roles of CXCR2 and its ligands in the development of the mouse, we examined the expression of MIP-2, KC, CXCR2, as well as the Duffy antigen binding protein for chemokines during embryonic (p.c.) days 11.5 through 14.5 in the mouse. We observed strong correlation between the expression of MIP-2 and CXCR2 in the developing brain, cardiovascular system and condensing mesenchyme between 11.5 and 13.5 days. Moreover, the expression of KC was parallel to the expression of the Duffy antigen binding protein for chemokines with regard to temporal pattern and tissue localization. MIP-2 and CXCR2 are highly expressed in the brain, first in the cerebellum and in the head mesenchyme, the meninges and the floor plate, and by 14.5 days are also present in the telencephalon, thalamus and hypothalamus. In the developing brain KC and Duffy were prominently expressed in the neuronal tracts, the forebrain, sympathetic ganglia, and along the periphery of the neural tube. However, KC and Duffy were less prevalent in the developing cardiovascular system, lung and other organs, muscle and bone, than are CXCR2 and MIP-2. These data suggest that the roles for these chemokines and their receptors during development may be more significant than was initially thought based upon the phenotype of the mice with targeted deletion of CXCR2 and Duffy.

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BMP4 is essential for lens induction in the mouse embryo

Cited by 410 publications

References 53 publications

Pax6 is misexpressed in Sox1 null lens fiber cells

Pax6 is misexpressed in Sox1 null lens fiber cells

Novel SOX2 partner-factor domain mutation in a four-generation family

Developmental Expression of Two CXC Chemokines, Mip-2 and Kc, and Their Receptors

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