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<jats:title>Variable Defenses</jats:title> <jats:p> Recent mapping of resistance alleles in the mosquito <jats:italic>Anopheles gambiae</jats:italic> that provide protection against the human malaria parasite <jats:italic>Plasmodium falciparum</jats:italic> revealed a major <jats:italic>Plasmodium</jats:italic> resistance island (PRI), comprising allelic versions of two leucine-rich repeat-containing proteins, LRIM1 and APL1, which form a complex with the complement C3-like protein TEP1. Using RNA interference inactivation of heterozygous allelic versions of <jats:italic>TEP1</jats:italic> genes, <jats:bold> Blandin <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="147" related-article-type="in-this-issue" vol="326" xlink:href="10.1126/science.1175241">147</jats:related-article> ) show that TEP1 heterogeneity reflects phenotypic variation among mosquito strains parasitized with the rodent malaria parasite <jats:italic>Plasmodium berghei</jats:italic> . It remains unclear whether the observed differences are the outcomes of different selection regimes, because of differing mechanisms, or because the complex is also used in other contexts. </jats:p>

<jats:title>Dog Coats Shed Genetic Secrets</jats:title> <jats:p> The coats of domestic dogs show great variation—long, short, straight, wavy, curly, wiry, or smooth. To investigate how this variation arises, <jats:bold> Cadieu <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="150" related-article-type="in-this-issue" vol="326" xlink:href="10.1126/science.1177808">150</jats:related-article> , published online 27 August) performed genome-wide association studies on 80 different dog breeds. The coat phenotype could be dissected into three simple traits of length, curl, and growth pattern or texture with each trait controlled by one major gene, <jats:italic>FGF5</jats:italic> (fibroblast growth factor-5), <jats:italic>KRT71</jats:italic> (keratin-71), and <jats:italic>RSPO2</jats:italic> (R-spondin-2), respectively. In combination, variants in these three genes alone account for the vast majority of the coat phenotypes in purebred dogs in the United States. Thus, a small number of simply inherited traits can be remixed to create extraordinary phenotypic variation. </jats:p>

<jats:title>Stemming Stem Cell Displacement</jats:title> <jats:p> Adult stem cell niches can contain multiple types of stem cells with coordinated regulation, but the mechanisms for these interactions are largely unknown. In the fruit fly testis, Janus kinase-signal transducer and activator of transcription (JAK-STAT) signaling is needed for the maintenance of the resident germline and somatic stem cells. The signaling inhibitor SOCS36E is a known JAK-STAT target. <jats:bold> Issigonis <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="153" related-article-type="in-this-issue" vol="326" xlink:href="10.1126/science.1176817">153</jats:related-article> ) now show that SOCS36E functions in the maintenance of the germline stem cell via suppression of JAK-STAT signaling, specifically in the somatic stem cells. This prevents the somatic stem cells from displacing neighboring germline stem cells in an integrin-dependent manner, allowing both stem cell populations to occupy the niche. </jats:p>

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