% pubman genre = article
@article{item_3587537,
title = {{Functional synergy of a human-specific and an ape-specific metabolic regulator in human neocortex development}},
author = {Xing, Lei and Gkini, Vasiliki and Nieminen, Anni I. and Zhou, Hui-Chao and Aquilino, Matilde and Naumann, Ronald and Reppe, Katrin and Tanaka, Kohichi and Carmeliet, Peter and Heikinheimo, Oskari and P{\"a}{\"a}bo, Svante and Huttner, Wieland B. and Namba, Takashi},
language = {eng},
issn = {2041-1723},
doi = {10.1038/s41467-024-47437-8},
year = {2024},
abstract = {{Metabolism has recently emerged as a major target of genes implicated in the evolutionary expansion of human neocortex. One such gene is the human-specific gene ARHGAP11B. During human neocortex development, ARHGAP11B increases the abundance of basal radial glia, key progenitors for neocortex expansion, by stimulating glutaminolysis (glutamine-to-glutamate-to-alpha-ketoglutarate) in mitochondria. Here we show that the ape-specific protein GLUD2 (glutamate dehydrogenase 2), which also operates in mitochondria and converts glutamate-to-$\alpha$KG, enhances ARHGAP11B{\textquoteright}s ability to increase basal radial glia abundance. ARHGAP11B + GLUD2 double-transgenic bRG show increased production of aspartate, a metabolite essential for cell proliferation, from glutamate via alpha-ketoglutarate and the TCA cycle. Hence, during human evolution, a human-specific gene exploited the existence of another gene that emerged during ape evolution, to increase, via concerted changes in metabolism, progenitor abundance and neocortex size.}},
journal = {{Nature Communications}},
volume = {15},
number = {1},
eid = {3468},
}