Highlights inDD

Abstract

Similar yet different (Dev Dyn 236:2493–2501) A mouse could never be mistaken for a chicken—unless their neural crests are being compared. Neural crest cells migrate from the neural tube to various tissues, where they differentiate into several cell types. Chick neural crest migration is under the control of bone morphogenetic proteins (BMPs). Seemingly in agreement, Bmp2 null mice lack migratory crest. But, is the mouse phenotype due to defects in migration or induction of crest fate? Correia et al. put this question to rest. Consistent with a role in migration, they show that early crest markers are induced in Bmp2 null embryos, but the cells remain associated with the neural tube. However, when they dig deeper, they find direct comparisons between mouse and chick neural crest falter. Whereas chick Cad6B is only expressed in premigratory crest, it is also in migratory crest in mouse. Additionally, unlike in chick, mouse neural crest Cad6B, Id2, and Wnt1 expression is not regulated by BMPs. The data illustrate that, although the top of the neural crest migration hierarchy is the same, downstream mechanisms differ. Not-so-“bad” cholesterol (Dev Dyn 236:2708–2712) Ever get a craving for fried food? You are not the only one. Work by Zhao and colleagues suggests that, at times, oligodendrocytes cannot get enough “bad” cholesterol either. Differentiated oligodendrocytes form a cholesterol-prich myelin sheath that enhances conduction of electrical signals along axons. One way that central nervous system glia procure cholesterol is by synthesizing their own. Here, the authors find evidence that the cells also uptake cholesterol from the surrounding environment. Mature oligodendrocytes express very low-density lipoprotein receptors (VLDLRs) and LDLRs in the spinal cord and brain, with some regional differences between the two. Highest expression of both receptors coincides with the peak of myelination in mouse spinal cords. These findings suggest that oligodendrocytes endocytose LDL and VLDL, and use them to build the myelin sheath. Apparently oligodendrocytes cannot get too much of a bad, er good, thing. Feast or famine? (Dev Dyn 236:2792–2799) In the face of an unpredictable food supply, the body's ability to adjust energy usage and storage is integral to survival. Energy homeostasis is a product of crosstalk between specific neurons in the hypothalamus and brainstem, and cues from the periphery, such as adipose tissue. Simon et al. show that, in the absence of the homeobox gene Sax2, these signals get crossed. Despite sufficient intake of food, energy stores in 2-week-old Sax2 null pups are depleted. They fail to incorporate lipids into white and brown adipose tissues, and liver glycogen stores and blood glucose levels are decreased. Consistent with a state of fasting, mRNA levels of neuropeptide Y in the hindbrain are low, whereas pro-opiomelanocortin levels are high. By contrast, serotonin mRNA levels are high, indicative of satiation. Because Sax2 is expressed in the brainstem close to serotonergic neurons, and not in affected peripheral tissues, the authors propose that the imbalance is due to dysregulation of central nervous system energy homeostasis signals by Sax2. Future studies promise to determine specifically where Sax2 fits into the energy homeostasis pathway.