Eye Field Specification in Xenopus laevis

Zuber, Michael E.

doi:10.1016/b978-0-12-385044-7.00002-3

Cited by 42 publications

(40 citation statements)

References 135 publications

(157 reference statements)

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“…1Bii-vii). However, because eye development is dependent on proper neural development (Fuhrmann, Harada et al, 2007, Zuber, 2010, it is likely that the eye defects may be a secondary manifestation of brain defects. Ventral Kv1.5 injections alone reduced (albeit non-significantly) the background incidence of brain phenotype in un-manipulated controls (Fig.…”

Section: Resultsmentioning

confidence: 99%

Local and long-range endogenous resting potential gradients antagonistically regulate apoptosis and proliferation in the embryonic CNS

Pai¹,

Lemire²,

Chen

et al. 2015

Int. J. Dev. Biol.

103

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-neural region). Together, the local and long-range bioelectric signals create a binary control system capable of fine-tuning apoptosis and proliferation with the brain and spinal cord to achieve correct pattern and size control. Our data suggest a roadmap for utilizing bioelectric state as a diagnostic modality and convenient intervention parameter for birth defects and degenerative disease states of the CNS.

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Section: Resultsmentioning

confidence: 99%

Local and long-range endogenous resting potential gradients antagonistically regulate apoptosis and proliferation in the embryonic CNS

Pai¹,

Lemire²,

Chen

et al. 2015

Int. J. Dev. Biol.

103

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“…The development of the retina, which is initiated during early stages of neurulation, begins with the expression of a combination of proteins known as eye-field transcription factors (Zuber et al, 2003;Zuber, 2010). Among these are the homeodomain transcription factor Rax, the homeodomain and paired domain protein Pax6, and the LIM-homeodomain protein Lhx2 (Zuber, 2010).…”

Section: Introductionmentioning

confidence: 99%

The stage-dependent roles of Ldb1 and functional redundancy with Ldb2 in mammalian retinogenesis

et al. 2016

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The Lim domain-binding proteins are key co-factor proteins that assemble with LIM domains of the LMO/LIM-HD family to form functional complexes that regulate cell proliferation and differentiation. Using conditional mutagenesis and comparative phenotypic analysis, we analyze the function of Ldb1 and Ldb2 in mouse retinal development, and demonstrate overlapping and specific functions of both proteins. Ldb1 interacts with Lhx2 in the embryonic retina and both Ldb1 and Ldb2 play a key role in maintaining the pool of retinal progenitor cells. This is accomplished by controlling the expression of the Vsx2 and Rax, and components of the Notch and Hedgehog signaling pathways. Furthermore, the Ldb1/Ldb2-mediated complex is essential for generation of earlyborn photoreceptors through the regulation of Rax and Crx. Finally, we demonstrate functional redundancy between Ldb1 and Ldb2. Ldb1 can fully compensate the loss of Ldb2 during all phases of retinal development, whereas Ldb2 alone is sufficient to sustain activity of Lhx2 in both early-and late-stage RPCs and in Müller glia. By contrast, loss of Ldb1 disrupts activity of the LIM domain factors in neuronal precursors. An intricate regulatory network exists that is mediated by Ldb1 and Ldb2, and promotes RPC proliferation and multipotency; it also controls specification of mammalian retina cells.

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“…For the eye to reach its normal size, neural progenitor cells of the anterior plate that eventually form the retina must remain pluripotent and continue to proliferate (reviewed in Zuber, 2010;Sinn and Wittbrodt, 2013). Tbx3 plays important roles in establishing and maintaining the pluri-and multipotency of stem and progenitor cells (Ivanova et al, 2006;Lee et al, 2007a;Lüdtke et al, 2009;Niwa et al, 2009;Han et al, 2010;Lu et al, 2011;Esmailpour and Huang, 2012).…”

Section: Repression Of Bmp Signaling During Neural Developmentmentioning

confidence: 99%

Tbx3 represses bmp4 expression and, with Pax6, is required and sufficient for retina formation

et al. 2016

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Vertebrate eye formation begins in the anterior neural plate in the eye field. Seven eye field transcription factors (EFTFs) are expressed in eye field cells and when expressed together are sufficient to generate retina from pluripotent cells. The EFTF Tbx3 can regulate the expression of some EFTFs; however, its role in retina formation is unknown. Here, we show that Tbx3 represses bmp4 transcription and is required in the eye field for both neural induction and normal eye formation in Xenopus laevis. Although sufficient for neural induction, Tbx3-expressing pluripotent cells only form retina in the context of the eye field. Unlike Tbx3, the neural inducer Noggin can generate retina both within and outside the eye field. We found that the neural and retina-inducing activity of Noggin requires Tbx3. Noggin, but not Tbx3, induces Pax6 and coexpression of Tbx3 and Pax6 is sufficient to determine pluripotent cells to a retinal lineage. Our results suggest that Tbx3 represses bmp4 expression and maintains eye field neural progenitors in a multipotent state; then, in combination with Pax6, Tbx3 causes eye field cells to form retina.

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Eye Field Specification in Xenopus laevis

Cited by 42 publications

References 135 publications

Local and long-range endogenous resting potential gradients antagonistically regulate apoptosis and proliferation in the embryonic CNS

Local and long-range endogenous resting potential gradients antagonistically regulate apoptosis and proliferation in the embryonic CNS

The stage-dependent roles of Ldb1 and functional redundancy with Ldb2 in mammalian retinogenesis

Tbx3 represses bmp4 expression and, with Pax6, is required and sufficient for retina formation

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