Cover Image

Abstract

Background: As the pituitary gland develops, signals from the hypothalamus are necessary for pituitary induction and expansion. Little is known about the control of cues that regulate early signaling between the two structures. Ligands and receptors of the Notch signaling pathway are found in both the hypothalamus and Rathke's pouch. The downstream Notch effector gene Hes1 is required for proper pituitary formation; however, these effects could be due to the action of Hes1 in the hypothalamus, Rathke's pouch, or both. To determine the contribution of hypothalamic Notch signaling to pituitary organogenesis, we used mice with loss and gain of Notch function within the developing hypothalamus. Results: We demonstrate that loss of Notch signaling by conditional deletion of Rbpj in the hypothalamus does not affect expression of Hes1 within the posterior hypothalamus or expression of Hes5. In contrast, expression of activated Notch within the hypothalamus results in ectopic Hes5 expression and increased Hes1 expression, which is sufficient to disrupt pituitary development and postnatal expansion. Conclusions: Taken together, our results indicate that Rbpj‐dependent Notch signaling within the developing hypothalamus is not necessary for pituitary development, but persistent Notch signaling and ectopic Hes5 expression in hypothalamic progenitors affects pituitary induction and expansion. Developmental Dynamics 244:921–934, 2015. © 2015 Wiley Periodicals, Inc.

Angiopoietin 1 and integrin beta 1b are vital for zebrafish brain development

“…In the hypothalamus, a high level of neurogenesis is continuously active, and the most representative neurotransmitter systems, including dopaminergic, GABAergic, histaminergic, and serotonergic neuron groups, are located there (Kaslin and Panula, 2001;Xie and Dorsky, 2017). Hypothalamic neurogenesis and patterning depend on several morphogen signals, including Notch/Delta signaling and wnt pathways, for establishing regional identity and functional circuitry (Aujla et al, 2015;Machluf et al, 2011). When angpt1 and itgb1b signaling is lacking, which causes impairments of notch and wnt pathways, we reasoned that the development of neuron populations in the hypothalamus might be affected.…”