Many biologically important processes, such as genetic differentiation, the spread of disease, and population stability, are affected by the (natural or enforced) subdivision of populations into networks of smaller, partly isolated, subunits. Such "metapopulations" can have extremely complex dynamics. We present a new general model that uses only two functions to capture, at the metapopulation scale, the main behavior of metapopulations. We show how complex, structured metapopulation models can be translated into our generalized framework. The metapopulation dynamics arising from some important biological processes are illustrated: the rescue effect, the Allee effect, and what we term the "antirescue effect." The antirescue effect captures instances where high migration rates are deleterious to population persistence, a phenomenon that has been largely ignored in metapopulation conservation theory. Management regimes that ignore a significant antirescue effect will be inadequate and may actually increase extinction risk. Further, consequences of territoriality and conspecific attraction on metapopulation-level dynamics are investigated. The new, simplified framework can incorporate knowledge from epidemiology, genetics, and population biology in a phenomenological way. It opens up new possibilities to identify and analyze the factors that are important for the evolution and persistence of the many spatially subdivided species.

No abstract

No abstract

No abstract

Duchenne Muscular Dystrophy (DMD) is a devastating genetic disease leading to degeneration of skeletal muscles and premature death. How dystrophin absence leads to muscle wasting remains unclear. Here, we describe an optimized protocol to differentiate human induced Pluripotent Stem Cells (iPSC) to a late myogenic stage. This allows to recapitulate classical DMD phenotypes (mislocalization of proteins of the Dystrophin-glycoprotein associated complex (DGC), increased fusion, myofiber branching, force contraction defects and calcium hyperactivation) in isogenic DMD-mutant iPSC lines in vitro. Treatment of the myogenic cultures with prednisolone (the standard of care for DMD) can dramatically rescue force contraction, fusion and branching defects in DMD iPSC lines. This argues that prednisolone acts directly on myofibers, challenging the largely prevalent view that its beneficial effects are due to anti-inflammatory properties. Our work introduces a new human in vitro model to study the onset of DMD pathology and test novel therapeutic approaches.