The Sexual Effect of Chicken Embryos on the Yolk Metabolites and Liver Lipid Metabolism

The metabolic processes of animals are usually affected by sex. Egg yolk is the major nutrient utilized for the growth and development of a chicken embryo. In this study, we explored the differences of yolk metabolites in male and female chicken embryos by LC–MS/MS. Furthermore, we investigated the mRNA expression of lipoprotein lipase (LPL) and fatty acid synthase (FAS) in chicken embryo liver with different sexes in different embryonic stages. The results showed that the nutrient metabolites in the yolk of female chickens were mainly related to lipid metabolism and amino acid metabolism in the early embryonic stage, and vitamin metabolism in the late embryonic stage. The male yolk metabolites were mainly associated with lipid metabolism and nucleic acid metabolism in the early developmental stage, and amino acids metabolism in the late embryonic stage. There was no significant difference in the expression of LPL or FAS in livers of male and female chicken embryos at different embryonic stages. Our results may lead to a better understanding of the sexual effect on yolk nutrient metabolism during chicken embryonic development.

Enhanced FGFR3 activity in post-mitotic principal neurons during brain development results in cortical dysplasia and axon miswiring

Abnormal levels of fibroblast growth factors (FGFs) and FGF receptors (FGFRs) have been detected in various neurological disorders. The potent impact of FGF-FGFR in multiple embryonic developmental processes makes it challenging to elucidate their roles in post-mitotic neurons. Taking an alternative approach, we directly examined the impact of aberrant FGFR function after neurogenesis by generating a FGFR gain-of-function (GOF) transgenic mouse which expresses constitutively activated FGFR3 (FGFR3K650E) in post-mitotic glutamatergic neurons. We found that enhanced FGFR activity in glutamatergic neurons results in abnormal radial migration and axonal miswiring. Regarding the lamination phenotype in GOF brains, we found later-born Cux1-positive neurons are dispersed throughout the GOF cortex. Such a cortical migration deficit is likely caused, at least in part, by a significant reduction of the radial processes normally projecting from the radial glia cells (RGCs). In addition, FGFR3 GOF also results in the misrouting of several long-range axonal projections, including the corpus callosum, anterior commissure, and postcommissural fornix. RNA-sequencing analysis of the GOF embryonic cortex reveals significant alterations in several pathways involved in cell cycle regulation and axonal pathfinding. Collectively, our results suggest that FGFR hyperfunction in post-mitotic neurons at the late embryonic stage result in cortical dysplasia and circuit miswiring.

Description of the first juvenile of Aegla franca Schmitt, 1942 (Crustacea, Decapoda, Aeglidae)

The post-embryonic development in Aegla franca is epimorphic, in which the hatching form is a juvenile that very much resembles the adults in general morphology. Newly-hatched juveniles were obtained under laboratory conditions from ovigerous females bearing eggs at late embryonic stage, and collected from the wild. Upon hatching, some juvenile specimens were cleared, stained, dissected and prepared for light microscopy on semi-permanent slides and each appendage was described in detail and illustrated accordingly. Some specimens were also prepared for scanning electron microscopy to obtain detailed information concerning setal morphology and ultrastructure of some cephalothoracic appendages. Comparison of the present results to previous descriptions of the first juvenile of other aeglid species show some interesting features observed only in Aegla franca. These features include the presence of pores on the first and second pairs of antennae; the rudimentary condition of the mandible and the long setae with a subterminal pore and scaly outgrowth distally on the basal bilobed endite of the maxilla.

Human multidrug resistance 3-P-glycoprotein expression in transgenic mice induces lens membrane alterations leading to cataract.

We have generated mice transgenic for a human multidrug resistance (MDR)3 mini-gene driven by a hamster vimentin promoter. The MDR3 gene encodes a P-Glycoprotein that resembles the mouse multidrug resistance 2 P-Glycoprotein shown to be involved in the translocation of the phospholipid phosphatidylcholine through the hepatocyte canalicular membrane (Smit et al., 1993. Cell. 75:451-462). The vimentin promoter drives expression of the MDR3 transgene in mesenchymal tissues and in the eye lens. We show here that the presence of human multidrug resistance 3 P-Glycoprotein in the lens results in a severe lenticular pathology. Lens structural abnormalities initiate at a late embryonic stage and increase during postnatal lens development. Differentiation of the primary fibers is affected, and the terminal differentiation of the lens epithelium into secondary fibers is also perturbed. The ultrastructural alterations, particularly of the lens plasma membranes, resemble those identified in congenital mouse osmotic cataract.