Phylogenetics has found its way into many different subdisciplines of biology, and has made lasting impacts in fields as disparate as community ecology and medicine. In evolutionary biology, the recent trend of phylogeny-oriented studies has been toward “scaling up”, and looking for very broad patterns in character evolution and diversification in attempts to make generalizations about the tempo and mode of evolution. This scaling up does come with a cost, in that we spend less time trying to understand how evolutionary processes work at the whole-organism level.

Evolutionary innovations are scattered throughout the tree of life, and have allowed the organisms that possess them to occupy novel adaptative zones. While the impacts of these innovations are well-documented, much less is known about how these innovations arise in the first place. Patterns of covariation among traits across macroevolutionary timescales can offer insights into the generation of innovation. However, to-date, there is no consensus on the role that trait covariation (i.e. integration and modularity) plays in this process.

Macroevolutionary studies of trait evolution are incomplete without the integration of speciation and extinction rates. The frequency of a character state on the tips of a phylogenetic tree is not only the result of the trait change per se but is also a function of lineage diversification if the character state is linked to speciation and extinction rates. In this talk, I will show three different examples of trait evolution linked to diversification.

The nucleus is extensively studied for its role in gene expression. However, growing evidences indicate that the biophysical properties of this organelle participate in cellular functions such as cell migration and pathogen killing; two processes critical for immune response. In this talk, I will describe our discovery of how immune cells undergoing confined migration squeeze their nuclei through narrow pores by forming a dense perinuclear actin network.

Mechanical deformations of DNA are ubiquitously part of universal biological processes involved in the transduction of genetic information. Although the average compliance of DNA to accommodate such deformations has been extensively measured, biophysical measurements of DNA have never been conducted on a genome-wide scale. Consequently, we lack experimental understanding of the extent to which the local mechanical properties of DNA vary with sequence along entire genomes, and how such variations modulate the energetics of diverse biological processes.

How simple tissues give rise to geometrically complex organs with robust shapes and functions is a fundamental question in biology with important implications in disease and translational medicine. The current mechanistic framework explains how upstream genetic and biochemical information pattern cellular mechanics and thereby tissue dynamics. In this framework, the main driving force is cell-intrinsic and generated by actomyosin contractility.

The long-term goal of the Kucenas Lab is to fundamentally understand the cellular and molecular mechanisms that mediate neural-glial and glial-glial interactions during nervous system development and injury/regeneration. Using Danio rerio (zebrafish) as a model system, we combine genetic and pharmacological perturbation, single cell manipulation, laser ablation/axotomy, small molecule screening, and in vivo, time-lapse imaging to directly and continuously observe glial cell origins, behaviors, and interactions in an intact vertebrate.

Population variation within Western Fence Lizards in the Puget Sound
By: Hayden Davis (Leaché Lab)

The role physical asymmetry plays in Drosophila neural stem cells
By: Melissa Delgado (Cabernard Lab)