Considering decoupled phenotypic diversification between ontogenetic phases in macroevolution: An example using Triggerfishes (Balistidae).

Across the Tree of Life, most studies of phenotypic disparity and diversification have been restricted to adult organisms. However, many lineages have distinct ontogenetic phases that differ from their adult forms in morphology and ecology. Focusing disproportionately on the evolution of adult forms unnecessarily hinders our understanding of the pressures shaping evolution over time. Non-adult disparity patterns are particularly important to consider for coastal ray-finned fishes, which often have juvenile phases with distinct phenotypes. These juvenile forms are often associated with sheltered nursery environments, with phenotypic shifts between adults and juvenile stages that are readily apparent in locomotor morphology. Whether this ontogenetic variation in locomotor morphology reflects a decoupling of diversification dynamics between life stages remains unknown. Here we investigate the evolutionary dynamics of locomotor morphology between adult and juvenile triggerfishes. We integrate a time-calibrated phylogenetic framework with geometric morphometric approaches and measurement data of fin aspect ratio and incidence, and reveal a mismatch between morphospace occupancy, the evolution of morphological disparity, and the tempo of trait evolution between life stages. Collectively, our results illuminate how the heterogeneity of morpho-functional adaptations can decouple the mode and tempo of morphological diversification between ontogenetic stages.

Translational regulation and protein-coding capacity of the 5' untranslated region of human TREM2.

TREM2 is a transmembrane receptor expressed in microglia and macrophages. Elevated TREM2 levels in these cells are associated with age-related pathological conditions, including Alzheimer's disease. However, the regulatory mechanism underlying the protein expression of TREM2 remains unclear. In this study, we uncover the role of the 5' untranslated region (5'-UTR) of human TREM2 in translation. An upstream start codon (uAUG) in the 5'-UTR of TREM2 is specific to some primates, including humans. The expression of the conventional TREM2 protein, starting from the downstream AUG (dTREM2), is repressed by the 5'-UTR in a uAUG-mediated manner. We also detect a TREM2 protein isoform starting from uAUG (uTREM2) that is largely degraded by proteasomes. Finally, the 5'-UTR is essential for the downregulation of dTREM2 expression in response to amino acid starvation. Collectively, our study identifies a species-specific regulatory role of the 5'-UTR in TREM2 translation.

Dietary protein restriction during pregnancy and/or early weaning reduces the number of goblet cells in the small and large intestines of female mice pups.

Background: It remains unclear whether goblet cell numbers in offspring are altered by maternal nutritional status and/or early weaning. Herein, using a murine model, we clarified whether a low-protein (LP) diet during pregnancy and/or early weaning changes villus structures, goblet cell numbers, mucin intensity, and mucin mRNA expression in the mucosal layer throughout the intestines in mice offspring. Methods: We examined villus-crypt structures and goblet cell numbers using hematoxylin-eosin staining. By performing alcian blue-PAS staining and RT-qPCR, we investigated mucin intensity in the mucosal layer and mRNA expressions of Muc2 and Muc4, respectively, in 17 (early weaning)-, 21 (normal weaning)- and 28-day old mice born from LP diet-fed mothers or those born from control diet-fed mothers during pregnancy. Results: Dietary protein restriction reduced goblet cell numbers in throughout the intestine, particularly in the duodenum and jejunum, and mucin intensity in the mucosal layer at the border of the jejunum and colon. The LP diet increased villus height and decreased villus thickness throughout the small intestine and crypt depth and width in the cecum and colon. Conclusions: Dietary protein restriction during pregnancy and/or early weaning decreased the number of goblet cells, mucin intensity in the mucosal layer, and the Muc2 and Muc4 mRNA expressions in the small and large intestines, and affected the villus and crypt structures in the small and large intestines in female offspring mice during and after weaning. General significance: Dietary abnormalities in fetal and weaning periods affects intestinal function.

Protein restriction during the fetal period upregulates IL1B and IL13 while suppressing Muc2 expression in the jejunum of mice after weaning.

OBJECTIVE: Several recent studies have suggested that malnutrition during developmental periods affects organ function, including that of the small intestine, after birth. However, it is unclear whether carbohydrate or protein restriction during pregnancy affects the expression of mucins and cytokines within the small intestine of offspring. METHODS: We examined mRNA and protein expression of cytokines and a Muc2 by quantitative reverse transcription polymerase chain reaction and Western blot, respectively, in the jejunoileum of 28- and 46-d-old mice born from mothers fed a low-carbohydrate (LC) or low-protein (LP) diet compared with those born from mothers fed a control diet during pregnancy. RESULTS: The mRNA and protein expressions of Il1b and Il13 in the jejunum in 28-d-old mice were higher in the LP group. Il1b mRNA expression in the jejunum in 46-d-old mice was higher in the LC and LP groups than in controls. The protein levels of mucin 2 in 46-d-old mice were lower in the LP group than in the control group. CONCLUSION: Fetal protein restriction in mice disrupts jejunal immune- and barrier function-related expression after weaning.