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https://www.selleckchem.com/products/hg6-64-1.html Although recombination is accepted to be common in bacteria, for many species robust phylogenies with well-resolved branches can be reconstructed from whole genome alignments of strains, and these are generally interpreted to reflect clonal relationships. Using new methods based on the statistics of single-nucleotide polymorphism (SNP) splits, we show that this interpretation is incorrect. For many species, each locus has recombined many times along its line of descent, and instead of many loci supporting a common phylogeny, the phylogeny changes many thousands of times along the genome alignment. Analysis of the patterns of allele sharing among strains shows that bacterial populations cannot be approximated as either clonal or freely recombining but are structured such that recombination rates between lineages vary over several orders of magnitude, with a unique pattern of rates for each lineage. Thus, rather than reflecting clonal ancestry, whole genome phylogenies reflect distributions of recombination rates.Shprintzen-Goldberg syndrome (SGS) is a multisystemic connective tissue disorder, with considerable clinical overlap with Marfan and Loeys-Dietz syndromes. These syndromes have commonly been associated with enhanced TGF-β signaling. In SGS patients, heterozygous point mutations have been mapped to the transcriptional co-repressor SKI, which is a negative regulator of TGF-β signaling that is rapidly degraded upon ligand stimulation. The molecular consequences of these mutations, however, are not understood. Here we use a combination of structural biology, genome editing, and biochemistry to show that SGS mutations in SKI abolish its binding to phosphorylated SMAD2 and SMAD3. This results in stabilization of SKI and consequently attenuation of TGF-β responses, both in knockin cells expressing an SGS mutation and in fibroblasts from SGS patients. Thus, we reveal that SGS is associated with an attenuation of TGF-

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