Ancient Sociology
Archaeology has used analysis of the artifacts and remains of people to uncover their past behaviors and to infer their cultural practices. However, establishing genetic relationships has only recently become possible. Mittnik et al. examined the kinship and inheritance of the remains of people from the German Lech River Valley over a time period spanning the Late Neolithic Corded Ware Culture, the Bell Beaker Complex, the Early Bronze Age, and the Middle Bronze Age (see the Perspective by Feinman and Neitzel). From genetic and archaeological analyses, it was revealed that the Early Bronze Age household's burials over multiple generations consisted of a high-status core family and unrelated low-status individuals. Furthermore, women were not related to the men within the household, suggesting that men stayed within their birth communities in this society, but women did not.
Science , this issue p. [731][1]; see also p. [682][2]
[1]: /lookup/doi/10.1126/science.aax6219
[2]: /lookup/doi/10.1126/science.aaz6574
Human Evolution
Neandertals clearly interbred with the ancestors of non-African modern humans, but many questions remain about our closest ancient relatives. Prufer et al. present a 30-fold-coverage genome sequence from 50,000- to 65,000-year-old samples from a Neandertal woman found in Vindija, Croatia, and compared this sequence with genomes obtained from the Altai Neandertal, the Denisovans, and ancient and modern humans (see the Perspective by Bergstrom and Tyler-Smith). Neandertals likely lived in small groups and had lower genetic diversity than modern humans. The findings increase the number of Neandertal variants identified within populations of modern humans, and they suggest that a larger number of phenotypic and disease-related variants with Neandertal ancestry remain in the modern Eurasian gene pool than previously thought.
Science , this issue p. [655][1]; see also p. [586][2]
[1]: /lookup/doi/10.1126/science.aao1887
[2]: /lookup/doi/10.1126/science.aaq0771
Neurogenetics
Gene expression changes and their control by accessible chromatin in the human brain during development is of great interest but limited accessibility. Trevino et al. avoided this problem by developing three-dimensional organoid models of human forebrain development and examining chromatin accessibility and gene expression at the single-cell level. From this analysis, they matched developmental profiles between the organoid and fetal samples, identified transcription factor binding profiles, and predicted how transcription factors are linked to cortical development. The researchers were able to correlate the expression of neurodevelopmental disease risk loci and genes with specific cell types during development.
Science , this issue p. [eaay1645][1]
[1]: /lookup/doi/10.1126/science.aay1645
Human Genomics
Genetic variants in parents may affect the fitness of their offspring, even if the child does not carry the allele. This indirect effect is referred to as “genetic nurture.” Kong et al. used data from genome-wide association studies of educational attainment to construct polygenic scores for parents that only considered the nontransmitted alleles (see the Perspective by Koellinger and Harden). The findings suggest that genetic nurture is ultimately due to genetic variation in the population and is mediated by the environment that parents create for their children.
Science , this issue p. [424][1]; see also p. [386][2]
[1]: /lookup/doi/10.1126/science.aan6877
[2]: /lookup/doi/10.1126/science.aar6429
Autism Genomics
About one-quarter of genetic variants that are associated with autism spectrum disorder (ASD) are due to de novo mutations in protein-coding genes. Brandler et al. wanted to determine whether changes in noncoding regions of the genome are associated with autism. They applied whole-genome sequencing to ∼2600 families with at least one affected child. Children with ASD had inherited structural variants in noncoding regions from their father. Regulatory regions of some specific genes were disrupted among multiple families, supporting the idea that a component of autism risk involves inherited noncoding variation.
Science , this issue p. [327][1]
[1]: /lookup/doi/10.1126/science.aan2261
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