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Science Papers Confirm Sitting Bull Descendent, Examine Mutation Accumulation in Aging

By analyzing a small amount of DNA obtained from the remains of Sitting Bull, scientists from the University of Copenhagen have confirmed an individual's claims that he is the great-grandson of the legendary Lakota Sioux leader. Sitting Bull was born in 1831 and led the Hunkpapa Lakota Sioux in their fight against the United States policies for Native Americans before being killed by Indian Police in 1890. An individual named Ernie LaPointe maintains that he is Sitting Bull's great-grandson and wanted to have this relationship confirmed. As reported in Science Advances, the scientists compared minor amounts of genomic data from a small piece of hair from Sitting Bull's scalp lock to genome-wide data from LaPointe and other Lakota Sioux using a new probabilistic approach, confirming LaPointe's claim. "To our knowledge, this is the first published example of a familial relationship between contemporary and a historical individual that has been confirmed using such limited amounts of ancient DNA across such distant relatives," the study's authors write. "With the advances in ancient DNA technology and the steady interest in samples from historical figures such as the Romanovs, Richard the III, and Jesse James, the new approach may help solve interesting questions within the fields of population genetics, history, and forensics." GenomeWeb has more on this, here.


Genome instability is a hallmark of aging, and various types of mutations have been shown to accumulate with age in different organs and tissues. However, a definite causal relationship between mutation accumulation and the aging process has thus far not been established. To investigate, a group led by scientists from the Albert Einstein College of Medicine used single-cell whole-genome sequencing to analyze the capacity of lung fibroblasts from four different rodent species of varying life spans, as well as humans, to maintain genome sequence integrity after treatment with a single dose of the chemotherapeutic agent bleomycin, which is known to induce both small deletions and base substitutions. "As predicted, the mutagen-induced mutation frequencies inversely correlated with species-specific maximum life span, with the greatest difference observed between the mouse and all other species," the study's authors write in Science Advances. "These results suggest that long-lived species may indeed be capable of processing DNA damage in a more accurate way than short-lived species." Additional studies will help confirm these findings as sequencing costs fall and robust reference genomes become available for additional species.