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Biology subjects

Spahr, S.

Publications and source records attributed to Spahr, S..

2 recordsLinked to original sources

Synergistic and antagonistic effects of chemical pollutants and parasitic fungi on cyanobacterial metabolism

Freshwater communities are increasingly impacted by anthropogenic pollutants, such as the widely used herbicide metolachlor (MET) and chemicals leached from cigarette butts (CBs), one of the most common types of litter worldwide. Cyanobacteria often interact with their parasitic chytrid fungi, which play a role in controlling their growth. Parasites represent an additional biotic stressor that can alter the effects of pollutants on their hosts. However, the metabolic responses of cyanobacteria to simultaneous exposure to pollutants and parasites remain poorly understood. In this study, we investigated the combined effects of abiotic (MET and CB leachate) and biotic (chytrid parasite Rhizophydium megarrhizum) stressors on the metabolic response of the toxigenic cyanobacterium Planktothrix agardhii. Co-exposure to MET and chytrids led to a synergistic effect, inducing oxidative stress, countered primarily by non-enzymatic mechanisms, whereas MET alone had no measurable effect. In contrast, CB leachate alone induced oxidative stress, but this effect was mitigated when cyanobacteria were also infected by chytrids, indicating an antagonistic interaction. This study demonstrates the complexity of cyanobacterial responses to interacting biotic and abiotic stressors and highlights the importance of considering host-parasite interactions in ecotoxicological assessments of cyanobacteria. A deeper understanding of how pollutants such as MET and CB leachate affect cyanobacteria-chytrid interactions at the metabolic level is crucial for evaluating their broader ecological impacts.

microbiology↗

Interaction of YAP with the Myb-MuvB (MMB) complex defines a transcriptional program to promote the proliferation of cardiomyocytes

The Hippo signalling pathway and its central effector YAP regulate proliferation of cardiomyocytes and growth of the heart. Using genetic models in mice we show that the increased proliferation of cardiomyocytes due to loss of the Hippo-signaling component SAV1 depends on the Myb-MuvB (MMB) complex. Similarly, proliferation of postnatal cardiomyocytes induced by constitutive active YAP requires MMB. Genome studies revealed that YAP and MMB regulate an overlapping set of cell cycle genes in cardiomyocytes. We find that YAP binds directly to B-MYB, a subunit of MMB, in a manner dependent on the YAP WW domains and a PPXY motif in B-MYB. Disruption of the interaction by overexpression of the YAP binding domain of B-MYB strongly inhibits the proliferation of cardiomyocytes. Our results point to MMB as a critical downstream effector of YAP in the control of cardiomyocyte proliferation.

molecular biology↗