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Kremer, A.

Publications and source records attributed to Kremer, A..

20 records · Page 2Linked to original sources

Secondary contacts between European white oaks reveal genes underlying reproductive isolation

AO_SCPLOWBSTRACTC_SCPLOWOaks are dominant forest tree species widely distributed across the Northern Hemisphere, where they constitute natural resources of economic, ecological, social and historical value. Hybridization and adaptive introgression have long been thought to be major drivers of their ecological success. Thus, the maintenance of species barriers remains a key question, given the extent of interspecific gene flow. In this study, we scanned the genomes of four European white oak species for reproductive barriers. We identified the ecological and phylogenic relationships of these species and inferred a long-term strict isolation followed by a recent and extensive postglacial contact. Then, we made use of the tremendous genetic variation among these species (31 million SNPs) to identify genomic regions for reproductive isolation. A literature-based functional annotation of the underlying genes highlighted important functions driving the reproductive isolation between these sister species. These functions were consistent with their ecological preferences and included tolerance to biotic and abiotic constraints. This study holds important implications for the renewal of European forests under global warming.

evolutionary biology↗

Sensory neuropathy-causing mutations in ATL3 cause aberrant ER membrane tethering

The ER is a complex network of sheets and tubules that is continuously being remodeled. The relevance of this membrane dynamics is underscored by the fact that mutations in Atlastins (ATL), the ER fusion proteins in mammals, cause neurodegeneration. How defects in this process disrupt neuronal homeostasis is largely unknown. Here we show by EM volume reconstruction of transfected cells, neurons and patient fibroblasts that the HSAN-causing ATL3 mutants promote aberrant ER tethering hallmarked by bundles of laterally attached ER tubules. In vitro, these mutants cause excessive liposome tethering, recapitulating the results in cells. Moreover, ATL3 variants retain their dimerization-dependent GTPase activity, but are unable to promote membrane fusion, suggesting a defect on an intermediate step of the ATL3 functional cycle. Our data therefore show that the effects of ATL3 mutations on ER network organization stretch beyond a loss of fusion, shedding a new light on neuropathies caused by atlastin defects.

cell biology↗