Reprogramming of trunk neural crest to a cranial crest-like identity alters their transcriptome and developmental potential.

Neural crest cells along the body axis of avian embryos differ in their developmental potential, such that the cranial neural crest forms cartilage and bone whereas the trunk neural crest is unable to do so. Previous studies have identified a cranial crest-specific subcircuit that can imbue the trunk neural crest with the ability to form cartilage after grafting to the head. Here, we examine transcriptional and cell fate changes that accompany this reprogramming.

The Effects of Acute Exercise on Short- and Long-Term Memory: Considerations for the Timing of Exercise and Phases of Memory.

The specific questions addressed from this research include: (1) Does high-intensity acute exercise improve memory?, (2) If so, do the mechanisms occur via encoding, consolidation, or retrieval? and (3) If acute exercise occurs in multiple phases of memory (e.g., before encoding and during consolidation), does this have an additive effect on memory? Three experimental, within-subject, counterbalanced studies were conducted among young adults.

Hnf4a Is Required for the Development of Cdh6-Expressing Progenitors into Proximal Tubules in the Mouse Kidney.

Background: Hepatocyte NF 4α (Hnf4a) is a major regulator of renal proximal tubule (PT) development. In humans, a mutation in impairs PT functions and is associated with Fanconi renotubular syndrome (FRTS). In mice, mosaic deletion of in the developing kidney reduces the population of PT cells, leading to FRTS-like symptoms.

Hnf4a deletion in the mouse kidney phenocopies Fanconi renotubular syndrome.

Different nephron tubule segments perform distinct physiological functions, collectively acting as a blood filtration unit. Dysfunction of the proximal tubule segment can lead to Fanconi renotubular syndrome (FRTS), with major symptoms such as excess excretion of water, glucose, and phosphate in the urine. It has been shown that a mutation in HNF4A is associated with FRTS in humans and that Hnf4a is expressed specifically in proximal tubules in adult rat nephrons.

Notch signaling promotes nephrogenesis by downregulating Six2.

During nephrogenesis, multipotent mesenchymal nephron progenitors develop into distinct epithelial segments. Each nephron segment has distinct cell types and physiological function. In the current model of kidney development, Notch signaling promotes the formation of proximal tubules and represses the formation of distal tubules.