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Nanba, K.

Publications and source records attributed to Nanba, K..

2 recordsLinked to original sources

Trapline foraging by nectar-collecting hornets

Central place foraging bees, butterflies, birds and bats are known to develop routes in order to visit familiar plant resources in a stable and repeatable order called "traplines". Here we report a similar behaviour in a social wasp, the Japanese yellow hornet Vespa simillima. We monitored the foraging movements of individually marked wild hornets collecting sucrose solution on four artificial flowers placed in the field. After thirty foraging bouts, all the hornets had developed a repeatable flower visitation sequence. Using two different arrays of flowers, we show how hornets increase their foraging efficiency through time but do not always use the shortest path to visit all flowers, often favoring movements between nearest neighbor flowers over global path optimization. Our study adds nectar-foraging wasps to the growing list of animals developing traplines thereby opening new perspectives for comparative cognition research.

animal behavior and cognition↗

Zinc transporter somatic gene mutations cause primary aldosteronism

Primary aldosteronism (PA) is the most common form of endocrine hypertension and effects one in 50 adults. PA is characterized by inappropriately elevated aldosterone production via renin-independent mechanisms. Driver somatic mutations for aldosterone excess have been found in approximately 90% of aldosterone-producing adenomas (APAs). Using next-generation sequencing, we identified recurrent in-frame deletions in SLC30A1 in five APAs (p.L51_A57del, n=3; p.L49_L55del, n=2). SLC30A1 encodes the ubiquitous zinc efflux transporter ZnT1 (zinc transporter 1). The identified SLC30A1 variants are situated in close proximity of the zincbinding site (H43 and D47) in transmembrane domain II and likely cause abnormal ion transport. PA cases with the unique SLC30A1 mutations showed male dominance and demonstrated increased aldosterone and 18-oxo-cortisol concentrations. Functional studies of the mutant SLC30A151_57del variant in a doxycycline-inducible adrenal cell system revealed abnormal Na+ conductivity caused by the mutant, which in turn led to the depolarization of the resting membrane potential, and thus to the opening of voltage-gated calcium channels. This resulted in an increase in cytosolic Ca2+ activity, which stimulated CYP11B2 mRNA expression and aldosterone production. Collectively, these data implicate the first-in-field zinc transporter mutations as a dominant driver of aldosterone excess in PA.

genetics↗