This is the blog for GW students taking Human Evolutionary Genetics. This site is for posting interesting tidbits on: the patterns and processes of human genetic variation;human origins and migration; molecular adaptations to environment, lifestyle and disease; ancient and forensic DNA analyses; and genealogical reconstructions.

GWHEG figure

GWHEG figure

Sunday, October 22, 2017

The Origin of Species: Homo sapiens Style

New DNA analysis of 2000 year old bones in South Africa points to an earlier emergence of Homo sapiens, from around 350-260kya, much earlier than the previously estimated 200kya. Through the use of mitochondrial DNA, researchers were able to use this data, along with a revised human mutation rate of 1.25e-8 per base pair per generation, to more accurately estimate the split of the Homo sapiens species. This analysis coincides with findings from another study conducted at the Jebel Irhoud site on fossil remains that estimated the origin of Homo sapiens to be ~300kya.

Diagram of emergence of Homo Sapiens

Tuesday, October 3, 2017

You Can Now Blame Paranthropus Boisei for Genital Herpes

Researchers Underdown, Kumar, and Houldcroft have proposed in a recent study that the robust australopithecine known as Paranthropus boisei might be the reason why genital herpes exists in the human population today.  Genetic analysis done by early researchers revealed that the virus that causes genital herpes, HSV2, is closer to the chimpanzee herpes variant, ChHV2, than it is to its counterpart HSV1 (cold sores).  Using that data, researchers hypothesized that HSV2 was not passed along to hominins from the last common ancestor of humans and chimpanzees, but across species lines later down in evolutionary history between 3 and 1.4 million years ago.  What Underdown, Kumar, and Houldcroft conclude, using the statistical analysis of temporal and spatial relationships between early hominins and ancestral chimpanzees, is that Paranthropus boisei represents the most important, and most plausable intermediate transmitter of the HSV2 into hominin populations.  You can, therefore, blame Zinj giving humans genital herpes.

Amanda Kunkle

Sunday, October 1, 2017

The Genetics of Staying in School

The article “The Genetics of Staying in School” from The Atlantic discusses a GWAS study done on 294,000 individuals from different areas of the world. The study found 74 gene variants that are associated with educational attainment. In other words, the people who have the variants, on average compete more formal schooling than individuals who do not have the variants. The Manhattan plot showed that there were big statistical differences on chromosomes 2, 3, 6, 9, 13, and 15, as well as some smaller differences on a few others. These kinds of studies can create a lot of public backlash, which is exactly what happened. Thus, the researchers also published a “Frequently Asked Questions” article discussing what the GWAS study really meant. The researchers explained that the 74 gene variants only accounted for 3 percent of the differences in education levels across the whole population. Thus, there are many other factors that affect educational attainment, and that nurture and nature go hand in hand when discussing educational success. However, this study will be helpful to social scientists who want to do educational studies about different styles of schooling in different populations.

Flu Season: Could a Protein Be Our Protection?

A recent study done at the University of Maryland School of Medicine discovered the potential ability of a protein known as RC-101 to protect against influenza and other diseases. RC-101 has been previously identified as a protective agent against disease in the animals in which it is found, such as Orangutans. Although the protein was lost in recent primate evolution and is not found in humans, researchers found similar benefits of viral protection when they studied the protein in the context of human immune cells as well as in mice. In human immune cells, they discovered that the protein not only blocked the virus from entering the target cell, but also stopped the inflammation that is responsible for symptoms associated with the flu, such as fever, lethargy, and pain. In mice, they studied two different groups: both groups received a dose of lethal influenza, but only the first group received the RC-101 protein. As a result, only 20% of mice in the first group died, whereas 90% of mice in the control group died. Ultimately, the flu is an ongoing issue causing thousands of deaths annually, despite the existence of vaccines. Based on the findings of this study, researchers now hope to incorporate this unique double function of RC-101 in making medicine for protection not just from the flu, but also a multitude of viral infections that stem from inflammation.

-Julie Thomasian 

Source: Eurkalert, Published 09/29/2017