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Biology subjects

Bek, L.

Publications and source records attributed to Bek, L..

2 recordsLinked to original sources

Microplastics Disrupt Predator-Induced Plasticity in Daphnia across Behavioral, Morphological and Molecular Levels

Microplastics (MP) are widespread in aquatic ecosystems and pose a threat to freshwater biodiversity. While numerous studies examine physiological effects on aquatic organisms, less is known about how MP alter chemically mediated interactions that regulate predator-prey dynamics. Predator-induced defenses in Daphnia depend on detecting kairomones and represent an important form of adaptive phenotypic plasticity. Whether MP interfere with these responses, and through which mechanisms, remains unclear. Here, we show that polystyrene MP impair predator-induced defenses across Daphnia species by disrupting predator-cue-mediated plasticity at the behavioral, morphological, and molecular levels. In D. longicephala, chronic exposure to PS fragments weakened Notonecta-induced morphological defenses, whereas additive-containing PS fragments nearly suppressed defense formation and reduced body size. Consistent with these phenotypic effects, proteomic analyses revealed alterations in pathways related to molting and chitin metabolism, linking MP exposure to impaired defense formation. In D. magna, PS particles attenuated fish kairomone-induced diel vertical migration, with stronger effects for larger particles, consistent with reduced effective availability or perception of predator cues. Natural limestone particles caused only minor effects, indicating particle-specific rather than general particle-driven responses. Our findings demonstrate that MP can disrupt adaptive predator-prey interactions with potential cascading consequences for freshwater food webs.

zoology↗

ACTN3 genotype influences skeletal muscle mass regulation and response to dexamethasone

Homozygosity for the common ACTN3 null polymorphism (ACTN3 577X) results in -actinin-3 deficiency in ~20% of humans worldwide and is linked to reduced sprint and power performance in both elite athletes and the general population. -Actinin-3 deficiency is also associated with reduced muscle mass and strength, increased risk of sarcopenia in the elderly, and altered response to muscle wasting induced by denervation and immobilisation. ACTN3 genotype is also a disease modifier for Duchenne muscular dystrophy (DMD), with -actinin-3 deficiency associated with slower disease progression. Here we show that -actinin-3 plays a key role in the regulation of protein synthesis and breakdown signalling in skeletal muscle, and its influence on muscle mass begins during early postnatal muscle development. Actn3 genotype also influences the skeletal muscle response to the glucocorticoid dexamethasone. Following acute dexamethasone exposure, transcriptomic analyses by RT-qPCR and RNA-sequencing show reduced atrophy signalling (Mstn, Tmem100, mRas, Fbxo32, Trim63) and anti-inflammatory response in -actinin-3 deficient mice compared to wild-type. -Actinin-3 deficiency also protects against muscle wasting following prolonged daily treatment with dexamethasone in female, but not male mice. In combination, these data suggest that ACTN3 R577X is a pharmacogenetic variant influencing the anti-inflammatory and muscle wasting response to glucocorticoid therapy.

genetics↗