Equilibrium bird species diversity in Atlantic islands

Half a century ago, MacArthur and Wilson proposed that the number of species on islands tends toward a dynamic equilibrium diversity around which species richness fluctuates [1]. The current prevailing view in island biogeography accepts the fundamentals of MacArthur and Wilson's theory [2] but questions whether their prediction of equilibrium can be fulfilled over evolutionary time-scales, given the unpredictable and ever-changing nature of island geological and biotic features [3-7]. Here we conduct a complete molecular phylogenetic survey of the terrestrial bird species from four oceanic archipelagos that make up the diverse Macaronesian bioregion-the Azores, the Canary Islands, Cape Verde, and Madeira [8, 9]. We estimate the times at which birds colonized and speciated in the four archipelagos, including many previously unsampled endemic and non-endemic taxa and their closest continental relatives. We develop and fit a new multi-archipelago dynamic stochastic model to these data, explicitly incorporating information from 91 taxa, both extant and extinct. Remarkably, we find that all four archipelagos have independently achieved and maintained a dynamic equilibrium over millions of years. Biogeographical rates are homogeneous across archipelagos, except for the Canary Islands, which exhibit higher speciation and colonization. Our finding that the avian communities of the four Macaronesian archipelagos display an equilibrium diversity pattern indicates that a diversity plateau may be rapidly achieved on islands where rates of in situ radiation are low and extinction is high. This study reveals that equilibrium processes may be more prevalent than recently proposed, supporting MacArthur and Wilson's 50-year-old theory

Identifizierung einer direkten Interaktion der Protein Kinase A mit dem L-Typ Ca2+ Kanal und Charakterisierung der Effekte von PDE3A Mutationen in auf Kardiomyozyten.

In the heart, the excitation-contraction coupling (ECC) pathway links excitation at the plasma membrane to contraction of the cardiomyocytes. The L-type Ca2+ channel (LTCC) and phosphodiesterase 3A (PDE3A) play important roles in this pathway by facilitating Ca2+ influx into the cytosol and hydrolysis of cAMP at subcellular compartments e.g. the sarcoplasmic reticulum (SR) and in the cytosol. Regulation of the LTCC opening is modulated by proteins found in its local environment, amongst them the catalytic subunit of PKA (PKA-CS). However, how PKA-CS is tethered to the channel is unclear. Recently, it was found that the GTP-binding protein Rad is associated with the LTCC and is blocking the pore-forming a1c subunit in the basal state (Liu et al., 2020). PKA phosphorylation of Rad in response to a-adrenergic stimulation leads to its dissociation from the channel complex, releasing the inhibitory effect. In the first part of this work, a novel interaction of PKA-CS with the C terminus of the a1c subunit is described. This interaction was mapped to two regulatory regions of a1c, the distal and the proximal regulatory domain (DCRD and PCRD). Mutating the DCRD and PCRD regions affected the interaction with PKA-CS in vitro but not in a cellular environment, pointing towards a complex regulatory mechanism involving several proteins or an alternative recruitment process. The two regions did not affect the enzymatic activity of PKA-CS. The LTCC and isoform 1 of PDE3A were found in a complex in HEK293 cells, however no further functional link could be found. In the second part of this thesis, effects of mutations in PDE3A were characterized. These mutations cause hypertension with brachydactyly type E (HTNB). Affected individuals experience progressive hypertension and have characteristic shorter metacarpals. If untreated, patients die before the age of 50. Surprisingly, their hearts do not show hypertension-induced cardiac damage. This points to a cardioprotective effect of PDE3A mutations. HiPSC-CMs expressing T445N or R862C PDE3A HTNB-causing substitutions were established and differentiated to cardiac myocytes as a model system to study Ca2+ cycling. The mutant cells showed lower PDE3A and the LTCC a1c subunit protein levels and a longer Ca2+ dwell time in the cytosol compared to the wild-type (WT) cells. This might be an adaptive mechanism to improve contractility of the cells that contributes to the cardioprotective effect of the mutations

BEAST trees Macaronesian birds

25 maximum clade crebility tree from BEAST analyses of Macaronesian birds; and information on models and molecular rates used

DAISIE model results for different taxonomic schemes

This file includes two tables showing the results of the optimizations of the 50 candidate models for the ‘conservative’ and ‘phylogenetic’ schemes, fitted to branching and colonisation times of birds of Macaronesia. Data from Valente et al. Current Biology