Biology subjects

Whitman, A.

Publications and source records attributed to Whitman, A..

4 recordsLinked to original sources

bioRxiv2025

Spatiotemporal dynamics of nearshore fish communities in Casco Bay, Maine

AO_SCPLOWBSTRACTC_SCPLOWNearshore regions in the Gulf of Maine are highly variable habitats acted upon by processes operating on multiple spatial scales and levels of biological organization. As such, they facilitate the reproduction, growth, and migration of many fish species, and are particularly tied to the life histories of many forage fishes. Temperatures in the Gulf of Maine have rapidly increased in recent decades, which may be driving changes in nearshore ecosystems. Here, we use 11 years of summer beach seine survey data within Casco Bay, Maine, to illustrate temperature-related changes to community structure. Further, we use Atlantic herring (Clupea harengus) and Atlantic silversides (Menidia menidia) as focal species to describe the effects of temperature on individual growth rates and relative abundance. The progression of seasonal use patterns and relative abundance in the nearshore with seasonal warming is evident; species that have cooler preferred temperatures are caught less frequently in the nearshore regions in late summer, when temperatures are highest. Increased temperatures were associated with significantly higher silverside growth rates and community compositions dominated by silverside. Temperature alone did not explain interannual variation in herring growth rates or predict herring-dominated nearshore community composition, and there is evidence that density-dependence may be more important to herring population dynamics. Monitoring nearshore ecosystems could provide critical insight into the dynamics of species that use these areas to facilitate reproduction, growth, and migration, and could therefore be used to identify potential changes to Gulf of Maine community and trophic ecology.

ecology↗

bioRxiv2025

A Multimodal Framework to Uncover Drug-Responsive Subpopulations in Triple-Negative Breast Cancer

Understanding how individual cancer cells adapt to drug treatment is a fundamental challenge limiting precision medicine cancer therapy strategies. While single-cell technologies have advanced our understanding of cellular heterogeneity, efforts to connect the behavior of individual cells to broader tumor drug responses and uncover global trends across diverse systems remain limited. There is a growing availability of single-cell and bulk omics data, but a lack of centralized tools and repositories makes it difficult to study drug response globally, especially at the level of single-cell adaptation. To address this, we present a multimodal framework that integrates bulk and single-cell treated and untreated transcriptomics data to identify drug responsive cell populations in triple-negative breast cancer (TNBC). Our framework leverages population-scale bulk transcriptomics data from TNBC samples to define seven main "identities", each representing unique combinations of biologically relevant genes. These identities are dynamic and trackable, allowing us to map them onto single cells and uncover global patterns of how cell populations respond to drug treatment. Unlike static classifications, this approach captures the evolving nature of cellular states, revealing that a select few identities dominate and drive population-level responses during treatment. Crucially, our ability to decode these trends through the inherent noise of single-cell data provides a clearer picture of how heterogeneous cell populations adapt to therapy. By identifying the dominant identities and their dynamics, we can better predict how entire tumors respond to treatment. This insight is essential for designing precise combination therapies tailored to the unique heterogeneity of patient tumors, addressing the single-cell variations that ultimately determine therapeutic outcomes.

bioinformatics↗

bioRxiv2020

Inhibition of Streptococcus pneumoniae autolysins highlight distinct differences between chemical and genetic inactivation

Despite renewed interest, development of chemical biology methods to study peptidoglycan metabolism has lagged in comparison to the glycobiology field in general. To address this, a panel of diamides were screened against the Gram-positive pathogen Streptococcus pneumoniae to identify inhibitors of bacterial growth. The screen identified the diamide fgkc as a narrow spectrum bacteriostatic inhibitor of S. pneumoniae growth with an MIC of 7.8 M. The diamide inhibited detergent-induced autolysis in a concentration dependent manner indicating peptidoglycan degradation as the mode-of-action. Genetic screening of autolysin mutants suggested LytB, an endo-N-acetylglucosaminidase, involved in cell division as the potential target. Surprisingly, biochemical, and phenotypic analysis contradicted the genetic screen results. Phenotypic studies with the{Delta} lytb strain illustrate the difference between genetic and chemical inactivation of autolysins. These findings suggest that meta-phenotypes including autolytic activity, cell morphology, and genetic screening can be the result of the complex interaction of one or more possible pathways that are connected to cell wall metabolism.

biochemistry↗

bioRxiv2019

Context-dependent role of vinculin in neutrophil adhesion, motility and trafficking

Neutrophils are innate immune effector cells that traffic from the peripheral blood to extravascular sites of inflammation. {beta}2 integrins are involved during multiple phases of neutrophil recruitment, including the transition from rolling to arrest, firm attachment and motility within the vasculature. Following neutrophil arrest, adhesion stabilization occurs as the neutrophil interacts with the endothelial surface and crawls into a favorable position for extravasation. The cytoskeletal protein vinculin has been implicated in other cell types as a regulator of adhesion strength by promoting focal adhesion maturation and as a sensor of the mechanical properties of the microenvironment. Neutrophils express vinculin but do not form mature focal adhesions. Here, we characterize the role of vinculin in {beta}2 integrin-dependent neutrophil adhesion, motility, mechanosensing, and recruitment. We observe that knockout of vinculin attenuates, but does not completely abrogate, neutrophil adhesion, spreading, and crawling under static conditions. In the presence of forces from fluid flow, vinculin was not required for neutrophil adhesion or migration. Vinculin deficiency only mildly attenuated neutrophil traction stresses and spreading on stiff, but not soft, polyacrylamide gels indicating a minor role for vinculin in the mechanosensing of the neutrophil as compared to slower moving mesenchymal cells that form mature focal adhesions. Consistent with these findings, we observe in vivo neutrophil recruitment into the inflamed peritoneum of mice remains intact in the absence of vinculin. Together, these data suggest that while vinculin regulates some aspects of neutrophil adhesion and spreading, it may be dispensable for neutrophil recruitment and motility in vivo.

immunology↗