Here, we have combined the analysis of vascular development in the mouse hindbrain with functional studies in primary human ECs, zebrafish embryos, and mouse retina to demonstrate that NRP1 is dispensable for the genetic specification of tip cells but essential for CDC42 activation.
These are consistent with the severe neurological features seen in the Nkx2-2 knockout mouse (Table 2) and Nkx2-2 bessentialntial for hindbrain development, ventral neuronal patterning, and oligodendrocyte differentiation (Briscoe et al., 1999; Qi et al., 2001).
This indicates a conserved role for Aldh enzymes in the production of RA required for hindbrain development in both zebrafish and mice.
This mean-independent noise control (MINC) mechanism is investigated in the context of an intracellular binding protein that regulates retinoic acid (RA) signaling during zebrafish hindbrain development.
We discuss the mouse hindbrain, forebrain and retina as widely used models to study developmental angiogenesis in the mammalian CNS and provide an overview of key cellular and molecular mechanisms regulating the vascularisation of these organs.
In mouse, a null mutation in the Aldh1a2 gene mimics the hindbrain phenotypes associated with full VAD, establishing Aldh1a2 as the main RA producing enzyme required in hindbrain development [29], [30], [50], [51].
The neural tube is strongly anteriorized and hindbrain development posterior to r4 is stopped.
Our results show that the compartment border coincides with the morphological boundary in the mouse hindbrain.
Histological analysis confirmed the presence of a hydrocephalus, revealed abnormal hindbrain development, and revealed retinal abnormalities (Fig. 6E, F, G).
6G and 6J, a colocalization of 5-HT and RGS4 in vivo was apparent in mouse hindbrain.
