Quantifying long‐term recurrence in planktonic microbial eukaryotes

How much temporal recurrence is present in microbial assemblages is still an unanswered ecological question. Even though marked seasonal changes have been reported for whole microbial communities, less is known on the dynamics and seasonality of individual taxa. Here, we aim at understanding microbial recurrence at three different levels: community, taxonomic group and operational taxonomic units (OTUs). For that, we focused on a model microbial eukaryotic community populating a long‐term marine microbial observatory using 18S rRNA gene data from two organismal size fractions: the picoplankton (0.2–3 µm) and the nanoplankton (3–20 µm). We have developed an index to quantify recurrence in particular taxa. We found that community structure oscillated systematically between two main configurations corresponding to winter and summer over the 10 years studied. A few taxonomic groups such as Mamiellophyceae or MALV‐III presented clear recurrence (i.e., seasonality), whereas 13%–19% of the OTUs in both size fractions, accounting for ~40% of the relative abundance, featured recurrent dynamics. Altogether, our work links long‐term whole community dynamics with that of individual OTUs and taxonomic groups, indicating that recurrent and non‐recurrent changes characterize the dynamics of microbial assemblages.     

Generalized spatial mark–resight models with incomplete identification: An application to red fox density estimates

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Deletion of MLIP (Muscle-enriched A-type Lamin-interacting Protein) Leads to Cardiac Hyperactivation of Akt/Mammalian Target of Rapamycin (mTOR) and Impaired Cardiac Adaptation

Aging and diseases generally result from tissue inability to maintain homeostasis through adaptation. The adult heart is particularly vulnerable to disequilibrium in homeostasis because its regenerative abilities are limited. Here, we report that MLIP (muscle enriched A-type lamin-interacting protein), a unique protein of unknown function, is required for proper cardiac adaptation. Mlip^−/− mice exhibited normal cardiac function despite myocardial metabolic abnormalities and cardiac-specific overactivation of Akt/mTOR pathways. Cardiac-specific MLIP overexpression led to an inhibition of Akt/mTOR, providing evidence of a direct impact of MLIP on these key signaling pathways. Mlip^−/− hearts showed an impaired capacity to adapt to stress (isoproterenol-induced hypertrophy), likely because of deregulated Akt/mTOR activity. Genome-wide association studies showed a genetic association between Mlip and early response to cardiac stress, supporting the role of MLIP in cardiac adaptation. Together, these results revealed that MLIP is required for normal myocardial adaptation to stress through integrated regulation of the Akt/mTOR pathways.