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Thread: We are 99.9% the same, therefore races don't exist23 days old

  1. #11
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    When will people understand that it's not about the genetic differences? It's about culture, values, beliefs and mentality which makes us all very different. It has nothing to do with race.

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  3. #12
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    The 0.1% difference actually makes a big difference in skin color, immune response and metabolism. 99.7% of modern human and Neanderthal DNA is exactly the same and as much as 2.6% of our DNA is from Neanderthals. DNA acquired from breeding with Neanderthals may explain why people of European descent respond differently to infection than those of African descent.

    Nédélec et al. (2016) measured how gene expression changed in response to the infection. About 30% of the approximately 12,000 genes that they tested were expressed differently between the two groups, even before infection. Many of the genes whose activity changed during the immune reaction had sequences that were very similar between Europeans and Neanderthals, but not Africans.

    Neanderthal ancestry makes up ∼2% of the ancestry of living humans found outside of Africa (Kelso and Prüfer, 2014). It is therefore plausible that interbreeding between Neanderthal and modern human populations could also contribute to some of the ancestry-related differences in gene expression we observed, especially if it enabled the ancestors of modern Europeans to more rapidly adapt to a new pathogen environment (Ségurel and Quintana-Murci, 2014). To test this hypothesis, we identified sites where the derived allele is shared between Neanderthals and non-African populations, but is absent in sub-Saharan Africans samples considered. This class of sites, which we call “Neanderthal-like sites” (NLS), is a conservative indicator of Neanderthal introgression (Sankararaman et al., 2014). Among the 18,862 NLS tested in our cis-QTL analyses, 297 were significantly associated with transcriptional variation of 145 genes (NLS-QTL). Among these 145 genes, 46% (FDR < 0.05) were differentially regulated in at least one experimental condition (non-infected, Listeria-infected, Salmonella-infected, or in the response to either type of infection) between Europeans and Africans (63% at a more relaxed FDR < 0.1). Thus, a non-negligible proportion of ancestry-related gene expression divergence probably results from introgression of functional Neanderthal variants into the ancestors of modern Europeans. Interestingly, some of these variants (n = 16) also have elevated iHS values (|iHS| ≥ 2) (Figure 5C; Table S5A) and therefore represent new candidates for adaptive introgression in humans.

    Together, our results provide a comprehensive characterization of genes for which the transcriptional responses of primary cells to live pathogenic bacteria differs depending on European versus African ancestry. We show that 34% of genes expressed in macrophages show at least one type of ancestry-related transcriptional divergence, whether in the form of differences in gene expression (30%), the transcriptional response to infection (9.3%), or, less commonly, differences in isoform usage (1%). Notably, the modest contribution of differences in isoform usage to ancestry-related expression levels differs from previous results in lymphoblastoid cell lines (LCLs), where they were found to be quite common (Lappalainen et al., 2013). The discrepancy between our results and those reported for LCLs may be related to differences in the experimental procedures used to produce the two sets of LCL lines, which were generated more than 20 years apart (Dausset et al., 1990).

    One of the most striking observations from our study was the markedly stronger response to infection induced in macrophages from individuals of African descent, particularly among inflammatory response genes. This result agrees with previous reports showing that AAs have higher frequencies of alleles associated with an increased pro-inflammatory response (Ness et al., 2004), increased levels of circulating C-reactive protein (Kelley-Hedgepeth et al., 2008), and a much higher rate of inflammatory diseases than EA individuals (Pennington et al., 2009). Although the exact causal link between ancestry and the pro-inflammatory response has yet to be established, we speculate that the stronger inflammatory response associated with African ancestry accounts for the increased ability of macrophages in African ancestry individuals to control bacterial growth post-infection.
    Last edited by ThirdTerm; 2018-06-07 at 19:46.

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