<i>belladonna</i>/(<i>lhx2</i>) is required for neural patterning and midline axon guidance in the zebrafish forebrain

Seth, Anandita; Culverwell, James; Walkowicz, Mitchell J.; Toro, Sabrina; Rick, Jens M.; Neuhauss, Stephan C. F.; Varga, Zoltán; Karlstrom, Rolf O.

doi:10.1242/dev.02390

Cited by 27 publications

(38 citation statements)

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“…Most studies on a LIM factor, Lhx2, have focused on its role in the development of the telencephalon and the eye. Recently, Lhx2 has been shown to be essential for diencephalon development in both the zebrafish and mice [102; 144]. In zebrafish, Lhx2 expression is found in the embryonic POA, a region that is diencephalic in origin [102].…”

Section: Fgf Signaling In the Presumptive Hypothalamusmentioning

confidence: 99%

“…Recently, Lhx2 has been shown to be essential for diencephalon development in both the zebrafish and mice [102; 144]. In zebrafish, Lhx2 expression is found in the embryonic POA, a region that is diencephalic in origin [102]. An interesting connection is that FGF signaling is required for the onset and maintenance of Lhx2 expression in zebrafish [102].…”

Section: Fgf Signaling In the Presumptive Hypothalamusmentioning

confidence: 99%

“…In zebrafish, Lhx2 expression is found in the embryonic POA, a region that is diencephalic in origin [102]. An interesting connection is that FGF signaling is required for the onset and maintenance of Lhx2 expression in zebrafish [102]. Application of FGFR antagonist SU5402 to zebrafish embryos reduces or eliminates Lhx2 expression in the diencephalon [102].…”

Section: Fgf Signaling In the Presumptive Hypothalamusmentioning

confidence: 99%

“…An interesting connection is that FGF signaling is required for the onset and maintenance of Lhx2 expression in zebrafish [102]. Application of FGFR antagonist SU5402 to zebrafish embryos reduces or eliminates Lhx2 expression in the diencephalon [102]. These zebrafish studies establish a clear link between FGF signaling and the development of the diencephalon.…”

Section: Fgf Signaling In the Presumptive Hypothalamusmentioning

confidence: 99%

“…As previously noted, FGF signaling is important for the expression and maintenance of the LIM homeobox gene, Lhx2 , in the zebrafish diencephalon, but infundibular development has not been examined in zebrafish lacking functional Lhx2 [102]. In contrast, Lhx2 mutant mice lack proper infundibular evagination, leading to defective infundibular and neurohypophysis formation.…”

Section: Fgf Signaling In the Presumptive Hypothalamusmentioning

confidence: 99%

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Fibroblast growth factor signaling in the developing neuroendocrine hypothalamus

Tsai

Brooks

Rochester

et al. 2011

Frontiers in Neuroendocrinology

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Fibroblast growth factor (FGF) signaling is pivotal to the formation of numerous central regions. Increasing evidence suggests FGF signaling also directs the development of the neuroendocrine hypothalamus, a collection of neuroendocrine neurons originating primarily within the nose and the ventricular zone of the diencephalon. This review outlines evidence for a role of FGF signaling in the prenatal and postnatal development of several hypothalamic neuroendocrine systems. The emphasis is placed on the nasally derived gonadotropin- releasing hormone neurons, which depend on neurotrophic cues from FGF signaling throughout the neurons' lifetime. Although less is known about neuroendocrine neurons derived from the diencephalon, recent studies suggest they also exhibit variable levels of dependence on FGF signaling. Overall, FGF signaling provides a broad spectrum of cues that ranges from genesis, cell survival/death, migration, morphological changes, to hormone synthesis in the neuroendocrine hypothalamus. Abnormal FGF signaling will deleteriously impact multiple hypothalamic neuroendocrine systems, resulting in the disruption of diverse physiological functions.

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Section: Fgf Signaling In the Presumptive Hypothalamusmentioning

confidence: 99%

Section: Fgf Signaling In the Presumptive Hypothalamusmentioning

confidence: 99%

Section: Fgf Signaling In the Presumptive Hypothalamusmentioning

confidence: 99%

Section: Fgf Signaling In the Presumptive Hypothalamusmentioning

confidence: 99%

Section: Fgf Signaling In the Presumptive Hypothalamusmentioning

confidence: 99%

See 3 more Smart Citations

Fibroblast growth factor signaling in the developing neuroendocrine hypothalamus

Tsai

Brooks

Rochester

et al. 2011

Frontiers in Neuroendocrinology

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Extrinsic factors as multifunctional regulators of retinal ganglion cell morphogenesis

Atkinson‐Leadbeater

McFarlane

2011

Developmental Neurobiology

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Neurons acquire a unique cell-type dependent morphology during development that is critical for their function in a neural circuit. The process involves a neuron sending out an axon that grows in a directed fashion to its target, and the elaboration of multiple, branched dendrites. The ultimate morphology of the neuron is sculpted by factors in the environment that act directly or indirectly to influence the behavior of the growing axon and dendrites. The output neuron of the retina, the retinal ganglion cell (RGC), has served as a useful model for the identification of molecular signals that control neuronal morphogenesis, because the entire development of the neuron, from the initiation of neurites to the establishment of synapses, is accessible for experimental manipulation and visualization. In this review we discuss data which argue that the visual system uses a limited number of signals to control RGC morphogenesis, with single molecules being reused multiple times to control distinct events in axon and dendrite outgrowth.

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Retinal axon guidance at the midline: Chiasmatic misrouting and consequences

Prieur

Rebsam

2017

Developmental Neurobiology

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The visual representation of the outside world relies on the appropriate connectivity between the eyes and the brain. Retinal ganglion cells are the sole neurons that send an axon from the retina to the brain, and thus the guidance decisions of retinal axons en route to their targets in the brain shape the neural circuitry that forms the basis of vision. Here, we focus on the choice made by retinal axons to cross or avoid the midline at the optic chiasm. This decision allows each brain hemisphere to receive inputs from both eyes corresponding to the same visual hemifield, and is thus crucial for binocular vision. In achiasmatic conditions, all retinal axons from one eye project to the ipsilateral brain hemisphere. In albinism, abnormal guidance of retinal axons at the optic chiasm leads to a change in the ratio of contralateral and ipsilateral projections with the consequence that each brain hemisphere receives inputs primarily from the contralateral eye instead of an almost equal distribution from both eyes in humans. In both cases, this misrouting of retinal axons leads to reduced visual acuity and poor depth perception. While this defect has been known for decades, mouse genetics have led to a better understanding of the molecular mechanisms at play in retinal axon guidance and at the origin of the guidance defect in albinism. In addition, fMRI studies on humans have now confirmed the anatomical and functional consequences of axonal misrouting at the chiasm that were previously only assumed from animal models. © 2016 Wiley Periodicals, Inc. Develop Neurobiol 77: 844-860, 2017.

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belladonna/(lhx2) is required for neural patterning and midline axon guidance in the zebrafish forebrain

Cited by 27 publications

References 0 publications

Fibroblast growth factor signaling in the developing neuroendocrine hypothalamus

Fibroblast growth factor signaling in the developing neuroendocrine hypothalamus

Extrinsic factors as multifunctional regulators of retinal ganglion cell morphogenesis

Retinal axon guidance at the midline: Chiasmatic misrouting and consequences

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