Symbiosis and horizontal gene transfer promote herbivory in the megadiverse leaf beetles.

Beetles that feed on the nutritionally depauperate and recalcitrant tissues provided by the leaves, stems, and roots of living plants comprise one-quarter of herbivorous insect species. Among the key adaptations for herbivory are plant cell wall-degrading enzymes (PCWDEs) that break down the fastidious polymers in the cell wall and grant access to the nutritious cell content. While largely absent from the non-herbivorous ancestors of beetles, such PCWDEs were occasionally acquired via horizontal gene transfer (HGT) or by the uptake of digestive symbionts.

Change Your Diet: How CO, Plant Phenology and Genotype Alter Grapevine Quality and Affect Performance and Larval Transcriptome of an Insect Herbivore.

Herbivorous insects need to cope with changing host plant biochemistry caused by abiotic and biotic impacts, to meet their dietary requirements. Larvae of the multivoltine European grapevine moth Lobesia botrana, one of the main insect pests in viticulture, feed on both flowers and berries. The nutritional value and defence compounds of these organs are changing with plant phenology and are affected by climate change which may accordingly alter plant-insect interactions.

Alternative splicing landscape in mouse skeletal muscle and adipose tissue: Effects of intermittent fasting and exercise.

Alternative splicing contributes to diversify the cellular protein landscape, but aberrant splicing is implicated in many diseases. To which extent mis-splicing contributes to insulin resistance as the causal defect of type 2 diabetes and whether this can be reversed by lifestyle interventions is largely unknown. Therefore, RNA sequencing data from skeletal muscle and adipose tissue of diabetes-susceptible NZO mice treated with or without intermittent fasting and of healthy C57BL/6J mice subjected to exercise were analyzed for alternative splicing differences using Whippet and rMATS.

A Novel Mouse Model for Cerebral Inflammatory Demyelination in X-Linked Adrenoleukodystrophy: Insights into Pathogenesis and Potential Therapeutic Targets.

Objective: X-linked adrenoleukodystrophy (ALD) is caused by mutations in ABCD1, a peroxisomal gene. More than half of males with an ABCD1 mutation develop inflammatory cerebral demyelination (cALD), but underlying mechanisms remain unknown and therapies are limited. We sought to develop and characterize a mouse model of cALD to facilitate study of disease mechanisms and therapy development.