Ovol2, a Mammalian Homolog of Drosophila ovo: Gene Structure, Chromosomal Mapping, and Aberrant Expression in Blind-Sterile Mice

Li, Bao-An; Dai, Qian; Li, Ling; Nair, Mahalakshmi; Mackay, Douglas R.; Dai, Xing

doi:10.1006/geno.2002.6831

Cited by 49 publications

(43 citation statements)

References 25 publications

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“…Recently, Li et al (2002a) reported two MOVO isoforms, named Ovol2A and Ovol2B, by compiling sequences of PCR-amplified cDNA fragments. Sequence comparison showed that Ovol2A was almost equivalent to MOVO-A, while Ovol2B was to MOVO-C.…”

Section: Discussionmentioning

confidence: 99%

Characterization of the isoforms of MOVO zinc finger protein, a mouse homologue of Drosophila Ovo, as transcription factors

Unezaki

Nishizawa

Okuda‐Ashitaka

et al. 2004

Gene

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Section: Discussionmentioning

confidence: 99%

Characterization of the isoforms of MOVO zinc finger protein, a mouse homologue of Drosophila Ovo, as transcription factors

Unezaki

Nishizawa

Okuda‐Ashitaka

et al. 2004

Gene

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“…Ovol2 Reinduces Central Components of the GRHL2 Network and Rescues TER and Lumen Expansion in Grhl2-Deficient Cells The gene encoding OVOL2, a mammalian homolog of Drosophila ovo, 26 was among the core targets of GRHL2. Deletion of Ovol2 in mice results in an embryonic phenotype and death by E10.5, 27 similar to the phenotype observed in Grhl2 mutant mice.…”

Section: Grhl2 Is Required For Lumen Expansion and Epithelial Barriermentioning

confidence: 99%

A Grainyhead-Like 2/Ovo-Like 2 Pathway Regulates Renal Epithelial Barrier Function and Lumen Expansion

Aue

Hinze

Walentin

et al. 2015

Journal of the American Society of Nephrology

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Grainyhead transcription factors control epithelial barriers, tissue morphogenesis, and differentiation, but their role in the kidney is poorly understood. Here, we report that nephric duct, ureteric bud, and collecting duct epithelia express high levels of grainyhead-like homolog 2 (Grhl2) and that nephric duct lumen expansion is defective in Grhl2-deficient mice. In collecting duct epithelial cells, Grhl2 inactivation impaired epithelial barrier formation and inhibited lumen expansion. Molecular analyses showed that GRHL2 acts as a transcriptional activator and strongly associates with histone H3 lysine 4 trimethylation. Integrating genome-wide GRHL2 binding as well as H3 lysine 4 trimethylation chromatin immunoprecipitation sequencing and gene expression data allowed us to derive a high-confidence GRHL2 target set. GRHL2 transactivated a group of genes including Ovol2, encoding the ovo-like 2 zinc finger transcription factor, as well as E-cadherin, claudin 4 (Cldn4), and the small GTPase Rab25. Ovol2 induction alone was sufficient to bypass the requirement of Grhl2 for E-cadherin, Cldn4, and Rab25 expression. Re-expression of either Ovol2 or a combination of Cldn4 and Rab25 was sufficient to rescue lumen expansion and barrier formation in Grhl2-deficient collecting duct cells. Hence, we identified a Grhl2/Ovol2 network controlling Cldn4 and Rab25 expression that facilitates lumen expansion and barrier formation in subtypes of renal epithelia. The renal collecting duct's vital electrolyte and waterregulatory functions are carried out by highly specialized cell populations. 1 The collecting duct itself is composed of a tight epithelium, which separates the urinary compartment from a hypertonic interstitium and maintains a barrier to concentration gradients. The collecting duct derives from the ureteric bud, which emanates from the nephric duct and then undergoes branching morphogenesis in response to signals from the adjacent metanephric mesenchyme. 2 Many of the genes that are critical for aspects of nephric duct development continue to be expressed in the ureteric bud and collecting duct, serving roles in development, differentiation, and maintenance of these cells (e.g., Pax2/8, Gata3, Emx2, and Hnf1b). 3 Little is known about the molecular pathways governing the specific epithelial properties of these cells, although it is clear that these epithelia share several cell biologic properties such as a uniform tubular appearance characterized by a cuboidal epithelium surrounding a fluid-filled lumen and a molecular composition of the apical junctional complex that includes

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“…4,5 OVOL2 expression has been also observed in murine and human epithelial tissues, such as skin and the germinal epithelium of the testes. 6 A molecular study of OVOL2 expression demonstrated that OVOL1 represses the activity of the OVOL2 promoter in a DNA-bindingedependent manner. 7 Furthermore, genetic deletion of OVOL1 up-regulates OVOL2 expression, leading to functional compensation by OVOL2, which suggests that OVOL1 negatively regulates OVOL2 expression.…”

mentioning

confidence: 99%

Activation of the OVOL1-OVOL2 Axis in the Hair Bulb and in Pilomatricoma

Ito

Tsuji

Ohno

et al. 2016

The American Journal of Pathology

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OVOL1 and OVOL2, ubiquitously conserved genes encoding C2H2 zinc finger transcription factors in mammals, control epithelial cell proliferation, and differentiation, including those in skin. OVOL1 and OVOL2 expression is coordinately mediated via the Wnt signaling pathway, and OVOL1 negatively regulates OVOL2 expression in a transcriptional manner. Our previous study of OVOL1 expression in human skin revealed that OVOL1 is preferentially expressed in the inner root sheath of the hair follicle. Therefore, we hypothesized that the OVOL1-OVOL2 axis is involved in normal and neoplastic follicular differentiation. Immunohistochemical analysis showed that OVOL1 and OVOL2 were strongly expressed in a mutually exclusive manner in the cytoplasm of inner root sheath cells and matrix cells, respectively, in normal follicles. OVOL2 was also expressed in pilomatricoma, with only partial expression of OVOL1. Cultured human keratinocytes expressed OVOL1 and OVOL2 on both the mRNA and protein levels. The expression of OVOL2 was higher in keratinocytes transfected with siRNA of OVOL1. Ketoconazole, a hair growth stimulant, up-regulated the expression of OVOL1 but did not affect OVOL2 expression. These results indicated that the OVOL1-OVOL2 axis may actively contribute to cell differentiation and proliferation in the hair bulb, suggesting that the OVOL1 and OVOL2 may be therapeutic targets of hair disorders, including alopecia, and play important roles in the tumorigenesis of pilomatricoma.

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Ovol2, a Mammalian Homolog of Drosophila ovo: Gene Structure, Chromosomal Mapping, and Aberrant Expression in Blind-Sterile Mice

Cited by 49 publications

References 25 publications

Characterization of the isoforms of MOVO zinc finger protein, a mouse homologue of Drosophila Ovo, as transcription factors

Characterization of the isoforms of MOVO zinc finger protein, a mouse homologue of Drosophila Ovo, as transcription factors

A Grainyhead-Like 2/Ovo-Like 2 Pathway Regulates Renal Epithelial Barrier Function and Lumen Expansion

Activation of the OVOL1-OVOL2 Axis in the Hair Bulb and in Pilomatricoma

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