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McDonald, C. L.

Publications and source records attributed to McDonald, C. L..

3 recordsLinked to original sources

Wax "tails" enable planthopper nymphs to self-right midair and land on their feet

The striking appearance of wax tails -- posterior wax projections on planthopper nymphs -- has captivated entomologists and naturalists alike. Despite their intriguing presence, the functional roles of these structures remain largely unexplored. This study leverages high-speed imaging to uncover the biomechanical implications of these wax formations in the aerial dynamics of planthopper nymphs (Ricania sp.). We quantitatively demonstrate that removing wax tails significantly increases body rotations during jumps. Specifically, nymphs without wax projections undergo continuous rotations, averaging 4.3 {+/-} 1.9 per jump, in contrast to wax-intact nymphs, who narrowly complete a full rotation, averaging only 0.7 {+/-} 0.2 per jump. This suggests that wax structures effectively counteract rotation through aerodynamic drag forces. These stark differences in body rotation correlate with landing success: nymphs with wax intact achieve a near perfect landing rate of 98.5%, while those without wax manage only a 35.5% success rate. Jump trajectory analysis reveals transitions from parabolic to Tartaglia shapes at higher take-off velocities for wax-intact nymphs, illustrating how wax structures assist nymphs in achieving stable, controlled descents. Our findings confirm the aerodynamic self-righting functionality of wax tails in stabilizing planthopper landings, advancing our understanding of the complex interplay between wax morphology and aerial maneuverability, with broader implications for the evolution of flight in wingless insects and bioinspired robotics.

bioengineering↗

H3K4 Methylation in β-cells Prevents Transcriptional Downregulation and Variance Associated with Type 2 Diabetes

Pancreatic {beta}-cells control glucose homeostasis via regulated production and secretion of insulin. This function arises from a highly specialized gene expression program which is established during development and then sustained, with limited flexibility, in terminally differentiated {beta}-cells. Dysregulation of this program is seen in type 2 diabetes (T2D) but mechanisms that preserve gene expression or underlie its dysregulation in mature {beta}-cells are not well resolved. Here we show that trithorax group-dependent histone H3 lysine 4 trimethylation (H3K4me3) maintains expression of genes important for insulin biosynthesis and glucose-responsiveness in {beta}-cells. Transcriptional changes in H3K4me3-deficient {beta}-cells lead to severe hyperglycemia in adult mice. We show that H3K4me3 deficiency leads to a less active and more repressed epigenome profile, which locally correlates with gene expression deficits but does not globally reduce gene expression. Instead, developmentally regulated genes and genes in weakly active or suppressed states particularly rely on H3K4 methylation. We then show that H3K4me3 is re-organized in diabetic Leprdb/db mouse islets in favour of weakly active and disallowed genes at the expense of terminal {beta}-cell markers with broad H3K4me3 peaks. Our results point to key roles of H3K4me3 in maintaining mature {beta}-cell function and establishing a dysfunctional transcriptome in diabetic islets.

cell biology↗

H3K4 trimethylation is required for postnatal pancreatic endocrine cell functional maturation

During pancreas development, endocrine progenitors differentiate into the islet-cell subtypes, which undergo further functional maturation in postnatal islet development. In islet {beta}-cells, genes involved in glucose-stimulated insulin secretion are activated and glucose exposure increases the insulin response as {beta}-cells mature. Here, we investigated the role of H3K4 trimethylation in endocrine cell differentiation and functional maturation by disrupting TrxG complex histone methyltransferase activity in mouse endocrine progenitors. In the embryo, genetic inactivation of TrxG component Dpy30 in NEUROG3+ cells did not affect the number of endocrine progenitors or endocrine cell differentiation. H3K4 trimethylation was progressively lost in postnatal islets and the mice displayed elevated random and fasting glycemia, as well as impaired glucose tolerance by postnatal day 24. Although postnatal endocrine cell proportions were equivalent to controls, islet RNA-sequencing revealed a downregulation of genes involved in glucose-stimulated insulin secretion and an upregulation of immature {beta}-cell genes. Comparison of histone modification enrichment profiles in NEUROG3+ endocrine progenitors and mature islets suggested that genes downregulated by loss of H3K4 trimethylation more frequently acquire active histone modifications during maturation. Taken together, these findings suggest that H3K4 trimethylation is required for the activation of genes involved in the functional maturation of pancreatic islet endocrine cells.

developmental biology↗