Talk:Neural - Epithalamus Development
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Cite this page: Hill, M.A. (2024, April 23) Embryology Neural - Epithalamus Development. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Talk:Neural_-_Epithalamus_Development |
2019
Wei L, Al Oustah A, Blader P & Roussigné M. (2019). Notch signaling restricts FGF pathway activation in parapineal cells to promote their collective migration. Elife , 8, . PMID: 31498774 DOI. Notch signaling restricts FGF pathway activation in parapineal cells to promote their collective migration
Abstract Coordinated migration of cell collectives is important during embryonic development and relies on cells integrating multiple mechanical and chemical cues. Recently, we described that focal activation of the FGF pathway promotes the migration of the parapineal in the zebrafish epithalamus. How FGF activity is restricted to leading cells in this system is, however, unclear. Here, we address the role of Notch signaling in modulating FGF activity within the parapineal. While Notch loss-of-function results in an increased number of parapineal cells activating the FGF pathway, global activation of Notch signaling decreases it; both contexts result in defects in parapineal migration and specification. Decreasing or increasing FGF signaling in a Notch loss-of-function context respectively rescues or aggravates parapineal migration defects without affecting parapineal cells specification. We propose that Notch signaling controls the migration of the parapineal through its capacity to restrict FGF pathway activation to a few leading cells. © 2019, Wei et al. KEYWORDS: FGF pathway; cell biology; collective cell migration; developmental biology; left right asymmetry; notch signaling; zebrafish PMID: 31498774 PMCID: PMC6733574 DOI: 10.7554/eLife.46275
2018
Liu B, Zhou K, Wu X & Zhao C. (2018). Foxg1 deletion impairs the development of the epithalamus. Mol Brain , 11, 5. PMID: 29394901 DOI.
Foxg1 deletion impairs the development of the epithalamus
Abstract The epithalamus, which is dorsal to the thalamus, consists of the habenula, pineal gland and third ventricle choroid plexus and plays important roles in the stress response and sleep-wake cycle in vertebrates. During development, the epithalamus arises from the most dorsal part of prosomere 2. However, the mechanism underlying epithalamic development remains largely unknown. Foxg1 is critical for the development of the telencephalon, but its role in diencephalic development has been under-investigated. Patients suffering from FOXG1-related disorders exhibit severe anxiety, sleep disturbance and choroid plexus cysts, indicating that Foxg1 likely plays a role in epithalamic development. In this study, we identified the specific expression of Foxg1 in the developing epithalamus. Using a "self-deletion" approach, we found that the habenula significantly expanded and included an increased number of habenular subtype neurons. The innervations, particularly the habenular commissure, were severely impaired. Meanwhile, the Foxg1 mutants exhibited a reduced pineal gland and more branched choroid plexus. After ablation of Foxg1 no obvious changes in Shh and Fgf signalling were observed, suggesting that Foxg1 regulates the development of the epithalamus without the involvement of Shh and Fgfs. Our findings provide new insights into the regulation of the development of the epithalamus. KEYWORDS: Choroid plexus; Epithalamus; FOXG1-related disorders; Fgf15; Habenula; Pineal gland; Sleep disturbance PMID: 29394901 PMCID: PMC5797387 DOI: 10.1186/s13041-018-0350-2
2014
Pitx2c ensures habenular asymmetry by restricting parapineal cell number
Development. 2014 Apr;141(7):1572-9. doi: 10.1242/dev.100305. Epub 2014 Mar 5.
Garric L1, Ronsin B, Roussigné M, Booton S, Gamse JT, Dufourcq P, Blader P. Author information
Abstract Left-right (L/R) asymmetries in the brain are thought to underlie lateralised cognitive functions. Understanding how neuroanatomical asymmetries are established has been achieved through the study of the zebrafish epithalamus. Morphological symmetry in the epithalamus is broken by leftward migration of the parapineal, which is required for the subsequent elaboration of left habenular identity; the habenular nuclei flank the midline and show L/R asymmetries in marker expression and connectivity. The Nodal target pitx2c is expressed in the left epithalamus, but nothing is known about its role during the establishment of asymmetry in the brain. We show that abrogating Pitx2c function leads to the right habenula adopting aspects of left character, and to an increase in parapineal cell numbers. Parapineal ablation in Pitx2c loss of function results in right habenular isomerism, indicating that the parapineal is required for the left character detected in the right habenula in this context. Partial parapineal ablation in the absence of Pitx2c, however, reduces the number of parapineal cells to wild-type levels and restores habenular asymmetry. We provide evidence suggesting that antagonism between Nodal and Pitx2c activities sets an upper limit on parapineal cell numbers. We conclude that restricting parapineal cell number is crucial for the correct elaboration of epithalamic asymmetry. KEYWORDS: Epithalamus, Left-right, Nodal, Parapineal, Pitx2, Zebrafish
PMID 24598158
