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Habte, B.

Publications and source records attributed to Habte, B..

2 recordsLinked to original sources

The environmental context of the Middle-to-Late Stone Age Transition in eastern Africa: seasonality as a key factor

In the transition between the Middle Stone Age (MSA) and the Late Stone Age (LSA) in eastern Africa, the archaeological record shows a gradual and asynchronous decline in MSA features and an increase in LSA characteristics. A link between this pattern and climatic variations has not yet been tested in the region using lithic attribute analysis. To investigate that, we integrated technological data of blades and bladelets from eastern African contexts (Marine Isotope Stages 5-1) with large-scale paleoclimatic reconstructions. A principal component analysis (PCA) finds the first component (reflecting artifacts dimensions) significantly correlating with time. This highlights a progressive reduction in size over time, a trend that has already been suggested for the MSA-LSA transition. The second principal component reflects artifact shape and shows a significant correlation with the marked aridity of the dry season (a common proxy for seasonality in tropical regions), with higher specialization observed in more humid areas. Based on this, we propose a new model where more variable blades reflect greater versatility in foraging strategies as adaptation to environments that become more challenging during part of the year. On the other hand, when it rains more during the dry season and differences through the year are milder, a more specialized toolkit with thinner, longer elements would emerge from refining and adapting to uniform and predictable situations and challenges.

evolutionary biology↗

Plural molecular and cellular mechanisms of pore domain KCNQ2 encephalopathy

KCNQ2 variants in children with neurodevelopmental impairment are difficult to assess due to their heterogeneity and unclear pathogenic mechanisms. We describe a child with neonatal-onset epilepsy, developmental impairment of intermediate severity, and KCNQ2 G256W heterozygosity. Analyzing prior KCNQ2 channel cryoelectron microscopy models revealed G256 as a node of an arch-shaped non-covalent bond network linking S5, the pore turret, and the ion path. Co-expression with G256W dominantly suppressed conduction by wild-type subunits in heterologous cells. Ezogabine partly reversed this suppression. G256W/+ mice have epilepsy leading to premature deaths. Hippocampal CA1 pyramidal cells from G256W/+ brain slices showed hyperexcitability. G256W/+ pyramidal cell KCNQ2 and KCNQ3 immunolabeling was significantly shifted from axon initial segments to neuronal somata. Despite normal mRNA levels, G256W/+ mouse KCNQ2 protein levels were reduced by about 50%. Our findings indicate that G256W pathogenicity results from multiplicative effects, including reductions in intrinsic conduction, subcellular targeting, and protein stability. These studies provide evidence for an unexpected and novel role for the KCNQ2 pore turret and introduce a valid animal model of KCNQ2 encephalopathy. Our results, spanning structure to behavior, may be broadly applicable because the majority of KCNQ2 encephalopathy patients share variants near the selectivity filter.

neuroscience↗