The spectral sensitivity of the visual system varies markedly between the fovea and surrounding periphery owing in part to the rapid fall in macular pigment density with eccentricity. We examined how colour appearance changes between the fovea and near periphery (8°) by measuring achromatic loci and the loci of unique and binary hues. Chosen colours remained much more similar at the two locations than predicted by the change in spectral sensitivity. Compensation for white may reflect long-term gain changes within the cones that equate sensitivity for the local average stimulus in the fovea and periphery. However, adjusting only to the average stimulus cannot correct for all of the effects of a spectral sensitivity change, and predicts differences in colour percepts between the fovea and periphery that were not observed. The similarities in hue percepts at 0 and 8° thus suggest that additional processes help compensate colour appearance to maintain constancy in the near periphery. We model the results of previous studies to show that similar adjustments are implied by age-related changes in lens pigment, and to show that these adjustments are consistent with previous measurements of peripheral colour appearance based on hue cancellation.
Aims:The mammalian gut is the largest endocrine organ. Dozens of hormones secreted by enteroendocrine cells regulate a variety of physiological functions of the gut but also of the pancreas and brain. Here, we examined the role of the helix-loop-helix transcription factor ID2 during the differentiation of intestinal stem cells along the enteroendocrine lineage.
Methods:To assess the functions of ID2 in the adult mouse small intestine, we used single-cell RNA sequencing, genetically modified mice, and organoid assays.
Results:We found that in the adult intestinal epithelium Id2 is predominantly expressed in enterochromaffin and peptidergic enteroendocrine cells.Consistently, the loss of Id2 leads to the reduction of Chromogranin A-positive enteroendocrine cells. In contrast, the numbers of tuft cells are increased in Id2 mutant small intestine. Moreover, ablation of Id2 elevates the numbers of Serotonin + enterochromaffin cells and Ghrelin + X-cells in the posterior part of the small intestine. Finally, ID2 acts downstream of BMP signalling during the differentiation of Glucagon-like peptide-1 + L-cells and Cholecystokinin + I-cells towards Neurotensin + PYY + N-cells. Conclusion: ID2 plays an important role in cell fate decisions in the adult small intestine. First, ID2 is essential for establishing a differentiation gradient for enterochromaffin and X-cells along the anterior-posterior axis of the gut. Next, ID2 is necessary for the differentiation of N-cells thus ensuring a differentiation gradient along the crypt-villi axis. Finally, ID2 suppresses the commitment of secretory intestinal epithelial progenitors towards tuft cell lineage and thus controls host immune response to commensal and parasitic microbiota.
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