Quintana-Murci and his colleagues also took advantage of a previously published map of areas of the human genome where Neanderthal genes are present, showing that innate immune genes are generally more likely to have been borrowed from Neanderthals than genes coding other types of proteins. Specifically, they noted that 126 innate immune genes in present-day Europeans, Asians, or both groups were among the top 5 percent of genes in the genome of each population most likely to have originated in Neanderthals. The cluster of toll-like receptor genes, encoding TLR 1, TLR 6, and TLR 10, both showed signs of having been borrowed from Neanderthals and having picked up adaptive mutations at various points in history.
Meanwhile, a group led by Janet Kelso of the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany, used both the same previously published Neanderthal introgression map that Quintana-Murci used and a second introgression map. The researchers searched for borrowed regions of the genome that were especially long and common in present-day humans, eventually zeroing in TLR6, TLR10, and TLR1. These receptors, which detect conserved microbial proteins such as flagellin, are all encoded along the same segment of DNA on chromosome four.
Vibrio harveyi is a marine bacteria that emits light only at high population density. The bacterial bioluminescence is controlled by a system called quorum sensing. In this system, signaling molecules are secreted, and when they bind to cell surface receptors, they turn on many genes, including those that produce bioluminescence.
A worldwide study of the DNA of 100,000 women has discovered two new genetic variants associated with an increased risk of breast cancer.
The genetic variants are specifically linked to the most common form of breast cancer, oestrogen receptor positive, and provide important insights into how the disease develops.
This flipped case study explores how the topics of membrane structure, transport, and signaling via membrane-bound receptors are intimately associated with the paralysis of muscle targeted by botulinum neurotoxin. The case scenario revolves around a fictitious socialite that has requested the assistance of her personal concierge physician with a condition that has developed after having participated in a Hamptons Botox party. The physician and a shadowing pre-med undergraduate chat about the molecular mechanisms behind Botox induced muscle paralysis. The case is designed as an engaging capstone exercise for students to gain appreciation for how knowledge of basic cellular and molecular biology mechanisms are essential for pharmaceutical development and medical patient diagnosis and prognosis. Written for an undergraduate general biology course, the case is also suitable for use in courses such as cellular biology, neurobiology, or human physiology.
This animation describes insulin resistance, an underlying cause of type 2 diabetes. It explains the roles of glucose and the hormone insulin in our body. Symptoms of diabetes are reviewed and various health complications that type 2 diabetes can lead to if left untreated.
UCSF Diabetes Center researchers explain the basics of both type 1 and type 2 diabetes. Faculty interviewed include Dr. Matthias Hebrok, Dr. Michael German, Dr. Suneil Koliwad, Dr. Stephen Gitelman.
UCSF Diabetes Center researchers explain the basics of both type 1 and type 2 diabetes. Faculty interviewed include Dr. Matthias Hebrok, Dr. Michael German, Dr. Suneil Koliwad, Dr. Stephen Gitelman.
DNA to Darwin allows 16-19 year-old school students to explore the molecular evidence for evolution through practical bioinformatics activities that use data analysis tools and molecular data.
Each of the activities on this web site centres around an engaging story from recent research in molecular genetics encompassing microbiology, plant and animal biology and human evolution.
Using an animal model for human PTSD, in which researchers conditioned mice to feel fear and then attempted to reverse it, the scientists found that blocking a single gene in mice could turn off their chronic fear response.