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<jats:title>Patterns of Early Migration</jats:title> <jats:p> In order to gain insight into various migrations that must have happened during movement of early humans into Asia and the subsequent populating of the largest continent on Earth, the <jats:bold>HUGO Pan-Asian SNP Consortium</jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" page="1541" related-article-type="in-this-issue" vol="326" xlink:href="10.1126/science.1177074">1541</jats:related-article> ) analyzed genetic variation in almost 2000 individuals representing 73 Asian and two non-Asian populations. The results suggest that there may have been a single major migration of people into Asia and a subsequent south-to-north migration across the continent. While most populations from the same linguistic group tend to cluster together in terms of relatedness, several do not, clustering instead with their geographic neighbors, suggesting either substantial recent mixing among the populations or language replacement. Furthermore, data from indigenous Taiwanese populations appear to be inconsistent with the idea of a Taiwan homeland for Austronesian populations. </jats:p>

<jats:title>Ghosts of Selection</jats:title> <jats:p> Glucose-6-phosphate dehydrogenase (G6PD) deficiency is the most common enzyme deficiency of humans, and it has been long suspected to exert an effect on <jats:italic>Plasmodium falciparum</jats:italic> malaria in Africa. Likewise, the increase in prevalence of the G6PD-Mahidol 487 <jats:sup>A</jats:sup> allele among Karen people in Thailand, who only in the past few thousand years have migrated into malarious zones, may be the result of selection by <jats:italic>Plasmodium vivax</jats:italic> malaria. <jats:italic>P. vivax</jats:italic> has recently been implicated in more severe disease than previously suspected, providing both a direct selective effect through mortality and an indirect selective effect through morbidity and reproductive failure. <jats:bold> Louicharoen <jats:italic>et al.</jats:italic> </jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" page="1546" related-article-type="in-this-issue" vol="326" xlink:href="10.1126/science.1178849">1546</jats:related-article> ) link population-genetic evidence for positive selection in an 8-year family-based study of 3000 Karen individuals and reveal that there is an association between the presence of the G6PD-Mahidol 487 <jats:sup>A</jats:sup> allele and a reduction in the density of <jats:italic>P. vivax</jats:italic> parasites circulating in the bloodstreams of infected individuals. The mutation appears to exert its effect on the physiology of immature red blood cells, which are the preferred niche for <jats:italic>P. vivax</jats:italic> but not of <jats:italic>P. falciparum</jats:italic> . </jats:p>

<jats:title>An Innervative Small RNA</jats:title> <jats:p> Amyotrophic lateral sclerosis (ALS) is a relentless disease characterized by progressive degeneration of motor neurons that control muscle movement, leading to muscle atrophy and paralysis. <jats:bold> Williams <jats:italic>et al.</jats:italic> </jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" page="1549" related-article-type="in-this-issue" vol="326" xlink:href="10.1126/science.1181046">1549</jats:related-article> ; see the Perspective by <jats:bold> <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="5959" page="1494" related-article-type="in-this-issue" vol="326" xlink:href="10.1126/science.1183842">Brown</jats:related-article> </jats:bold> ) show that a small noncoding RNA that is selectively expressed in skeletal muscle, miR-206, senses motor neuron injury or loss and helps ameliorate resultant muscle damage by promoting regeneration of neuromuscular synapses. Expression of miR-206 was dramatically induced in a mouse model of ALS, and when this RNA was removed from mice by genetic manipulation, the disease progressed at a faster rate. The salutary effects of miR-206 appear to be mediated through a signaling pathway in muscle cells involving histone deacetylase 4 and a fibro-blast growth factor modulator, activation of which leads to release of factors that promote nerve-muscle interactions. </jats:p>

<jats:title>Norbin Knockout</jats:title> <jats:p> Metabotropic glutamate receptors (mGluRs) are critical neurotransmitter sensors implicated in central neuronal functions like learning and memory and in diseases of the nervous system. <jats:bold> Wang <jats:italic>et al.</jats:italic> </jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" page="1554" related-article-type="in-this-issue" vol="326" xlink:href="10.1126/science.1178496">1554</jats:related-article> ) searched for proteins that interact with mGluR5a and identified a previously unrecognized component of the receptor signaling complex. The protein Norbin directly interacted with the receptor. Loss of Norbin in mice or cultured cells showed that it is necessary for the accumulation of mGluR5a in the cell membrane, for normal modulation of synaptic plasticity, and for some behavioral responses. </jats:p>

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