Lifeboat Foundation

The human genome contains billions of pieces of information and around 22000 genes, but not all of it is, strictly speaking, human. Eight percent of our DNA consists of remnants of ancient viruses, and another 40 percent is made up of repetitive strings of genetic letters that is also thought to have a viral origin. Those extensive viral regions are much more than evolutionary relics: They may be deeply involved with a wide range of diseases including multiple sclerosis, hemophilia, and amyotrophic lateral sclerosis (ALS), along with certain types of dementia and cancer.

For many years, biologists had little understanding of how that connection worked—so little that they came to refer to the viral part of our DNA as dark matter within the genome. “They just meant they didn’t know what it was or what it did,” explains Molly Gale Hammell, an associate professor at Cold Spring Harbor Laboratory. It became evident that the virus-related sections of the genetic code do not participate in the normal construction and regulation of the body. But in that case, how do they contribute to disease?

Eight percent of our DNA consists of remnants of ancient viruses, and another 40 percent is made up of repetitive strings of genetic letters that is also thought to have a viral origin.

Previous studies have shown that AgRP neurons in the arcuate nucleus (ARC) respond to energy deficits and play a key role in the control of feeding behavior and metabolism. Here, we demonstrate that chronic unpredictable stress, an animal model of depression, decreases spontaneous firing rates, increases firing irregularity and alters the firing properties of AgRP neurons in both male and female mice. These changes are associated with enhanced inhibitory synaptic transmission and reduced intrinsic neuronal excitability. Chemogenetic inhibition of AgRP neurons increases susceptibility to subthreshold unpredictable stress. Conversely, chemogenetic activation of AgRP neurons completely reverses anhedonic and despair behaviors induced by chronic unpredictable stress.

The adeno-associated viruses often used as vectors to deliver gene therapy can trigger unwanted and sometimes dangerous immune responses. Now, a Harvard University team led by renowned geneticist George Church, Ph.D., has developed a way to “cloak” AAVs from immune surveillance. They’ve spun off Ally Therapeutics to develop it.

After tracing the origins of schizophrenia to genes expressed in the placenta while in utero, scientists have now zeroed in on the combination of risk factors that could predict which infants are at greatest risk of developing the condition later in life.

The findings reinforce an emerging picture of schizophrenia as a genetic disorder, with a fate determined by complications that can arise during pregnancy.

Researchers from the Lieber Institute for Brain Development at Johns Hopkins University and the University of North Carolina in the US analysed the relationship between key genes and cognitive development in the first few years after birth.

Although wireless optogenetic technologies enable brain circuit investigation in freely moving animals, existing devices have limited their full potential, requiring special power setups. Here, the authors report fully implantable optogenetic systems that allow intervention-free wireless charging and controls for operation in any environment.

Circulating branched-chain amino acids (BCAAs) are elevated in obesity and diabetes, and recent studies support a causal role for BCAAs in insulin resistance and defective glycemic control. The physiological mechanisms underlying BCAA regulation are poorly understood. Here we show that insulin signaling in the mediobasal hypothalamus (MBH) of rats is mandatory for lowering plasma BCAAs, most probably by inducing hepatic BCAA catabolism. Insulin receptor deletion only in agouti-related protein (AgRP)–expressing neurons (AgRP neurons) in the MBH impaired hepatic BCAA breakdown and suppression of plasma BCAAs during hyperinsulinemic clamps in mice. In support of this, chemogenetic stimulation of AgRP neurons in the absence of food significantly raised plasma BCAAs and impaired hepatic BCAA degradation.

SARS-CoV-2 mutations similar to those in the B1.1.7 UK variant could arise in cases of chronic infection, where treatment over an extended period can provide the virus multiple opportunities to evolve, say scientists.

Writing in Nature, a team led by Cambridge researchers report how they were able to observe SARS-CoV-2 mutating in the case of an immunocompromised patient treated with convalescent plasma. In particular, they saw the emergence of a key mutation also seen in the new variant that led to the UK being forced once again into strict lockdown, though there is no suggestion that the variant originated from this patient.

Using a synthetic version of the virus Spike protein created in the lab, the team showed that specific changes to its genetic code — the mutation seen in the B1.1.7 variant — made the virus twice as infectious on cells as the more common strain.

As far as ‘compiling’ this into a human — I definitely don’t see the path to that.

Analysis reveals genetic control elements that are linked to hundreds of human traits.

Twenty years ago this month, the first draft of the human genome was publicly released. One of the major surprises that came from that project was the revelation that only 1.5 percent of the human genome consists of protein-coding genes.

Over the past two decades, it has become apparent that those noncoding stretches of DNA, originally thought to be “junk DNA,” play critical roles in development and gene regulation. In a new study published on February 32021, a team of researchers from MIT has published the most comprehensive map yet of this noncoding DNA.