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Rhodes, L.

Publications and source records attributed to Rhodes, L..

2 recordsLinked to original sources

A catastrophic marine mortality event caused by a complex algal bloom including the novel brevetoxin producer, Karenia cristata (Dinophyceae)

Harmful algal blooms of Karenia brevis (Dinophyceae) are a global anomaly, occurring in one location worldwide, causing severe marine and acute human impacts via brevetoxins (BTX). During 2025 an unprecedented, currently ongoing, mass marine mortality occurred in South Australia, across an area of [~]20,000 km2, persisting for >6 months, resulting in the deaths of [~]106 marine animals of >550 taxa, with human health impacts. Using custom metabarcoding, long-read sequencing and targeted quantitative PCR, we characterized the microalgal assemblage. Karenia cristata dominated over the sampling area, in an assemblage with four other Karenia species with varied abundances spatially and temporally. High abundances of K. cristata appeared in the austral autumn, and hydrodynamic processes appear to have entrained cells coastward in the semi-enclosed seas. We isolated the species and characterized it using light and electron microscopy, liquid chromatography mass spectrometry and toxicity assays. We show for the first time that the rare and little known K. cristata produces significant BTX with a profile (BTX-2, -3, -B5), differing from K. brevis, with toxicological effects. These findings reveal a novel, significant BTX-producing Karenia, which considering its substantial detrimental marine ecosystem impacts, is an emerging international threat with unknown consequences in changing ocean conditions.

ecology↗

Cancer cells resist mechanical destruction in the circulation via RhoA-myosin II axis

During metastasis cancer cells are exposed to potentially destructive hemodynamic forces including fluid shear stress (FSS) while en route to distant sites. However, prior work indicates that cancer cells are more resistant to brief pulses of high-level fluid shear stress (FSS) in vitro relative to non-transformed epithelial cells. Herein we identify a mechanism of FSS resistance in cancer cells, and extend these findings to mouse models of circulating tumor cells (CTCs). We show that cancer cells acutely isolated from primary tumors are resistant to FSS. Our findings demonstrate that cancer cells activate the RhoA-myosin II axis in response to FSS, which protects them from FSS-induced plasma membrane damage. Moreover, we show that the myosin II activity is protective to CTCs in mouse models. Collectively our data indicate that viable CTCs actively resist destruction by hemodynamic forces and are likely to be more mechanically robust than is commonly thought.

cancer biology↗