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Updated: 47 weeks 6 days ago
Fishing boats at the harbor in Luderitz, Namibia. The small town is known for its crayfish industry. New groundbreaking research shows that with improved fishing approaches -- compared to business as usual -- the majority of the world's wild fisheries could be at healthy levels in just 10 years and global fish populations could double by 2050.
Bacteria are the most abundant form of life on Earth, and they are capable of living in diverse habitats ranging from the surface of rocks to the insides of our intestines. Over millennia, these adaptable little organisms have evolved a variety of specialized mechanisms to move themselves through their particular environments. In two recent Caltech studies, researchers used a state-of-the-art imaging technique to capture, for the first time, three-dimensional views of this tiny complicated machinery in bacteria.
According to epigenetics -- the study of inheritable changes in gene expression not directly coded in our DNA -- our life experiences may be passed on to our children and our children's children. Studies on survivors of traumatic events have suggested that exposure to stress may indeed have lasting effects on subsequent generations. But how exactly are these genetic "memories" passed on?
Tardigrades have not acquired a significant proportion of their DNA from other organisms, a new study shows. Tardigrades, also known as moss piglets or water bears, are eight-legged microscopic animals that have long fascinated scientists for their ability to survive extremes of temperature, pressure, lack of oxygen, and even radiation exposure.
Kent Bradford, left, and Alfred Huo, seen here with a flowering lettuce plant, found that lettuce could be prevented from flowering by increasing the expression of a specific microRNA Like most annuals, lettuce plants live out their lives in quiet, three-act dramas that follow the seasons. Seed dormancy gives way to germination; the young plant emerges and grows; and finally in the climax of flowering, a new generation of seeds is produced. It's remarkably predictable, but the genetics that coordinates these changes with environmental cues has not been well understood.
Space-filling model of Reb1 bound to DNA. In a study published on 28 March 2016 in the Proceedings of the National Academy of Sciences, researchers at the Medical University of South Carolina (MUSC) and Virginia Commonwealth University have resolved the first protein structure in a family of proteins called transcription terminators. The crystal structure of the protein, called Reb1, provides insight into aging and cancer, according to Deepak Bastia, Ph.D., Endowed Chair for Biomedical Research in the MUSC Department of Biochemistry and Molecular Biology and co-senior author of the study.
New research by Dr. Sylvie Lesage, scientist at Maisonneuve-Rosemont Hospital (CIUSSS- East Montreal) and associate research Professor at University of Montreal, just published in the prestigious international scientific journal Nature Genetics, has discovered that a common genetic defect in beta cells may underlie both known forms of diabetes.
This image shows TFIID (blue) as it contacts the DNA and recruits the polymerase (grey) for gene transcription. The start of the gene is shown with a flash of light. Your DNA governs more than just what color your eyes are and whether you can curl your tongue. Your genes contain instructions for making all your proteins, which your cells constantly need to keep you alive. But some key aspects of how that process works at the molecular level have been a bit of a mystery--until now.
Female orphan chimpanzee are cared for at the Sanaga-Yong Chimpanzee Rescue Center. Understanding the origins of emerging diseases - as well as more established disease agents -- is critical to gauge future human infection risks and find new treatment and prevention approaches. This holds true for malaria, which kills more than 500,000 people a year. Symptoms, including severe anemia, pregnancy-associated malaria, and cerebral malaria, have been linked to the parasite's ability to cause infected red blood cells to bind to the inner lining of blood vessels.
In eLife today (22 March), Wellcome Trust Sanger Institute scientists show how the parasite responsible for the neglected tropical disease Black Fever (visceral leishmaniasis) can become resistant to drug treatment. Studying the whole genomes of more than 200 samples of Leishmania donovani revealed that the addition of just two bases of DNA to a gene known as LdAQP1 stops the parasite from absorbing antimonial drugs.
The cost of treating hepatitis C virus (HCV) could be cut up to 50 percent if mathematical models are used to predict when patients can safely stop taking direct-acting antiviral (DAA) medication, according to a new study by researchers at Loyola University Health System and Loyola University Chicago.
The authors investigated the effects of 15,000 genes on the balance between self-renewal and differentiation of the human blood stem cell (blue box). An important element in getting blood stem cells to multiply outside the body is to understand which of the approximately 20 000 genes in the human body control their growth. A research team at Lund University in Sweden has studied close to 15 000 of these genes alongside each other. The researchers have succeeded in identifying four key genes which, together, govern the growth and multiplication of the stem cells. The study is now being published in the journal Cell Reports.
Every cell on the surface of this genetically engineered zebrafish expresses a unique combination of green, red and blue fluorescent proteins, resulting in over 70 different hues Scientists can now watch how hundreds of individual cells work together to maintain and regenerate skin tissue, thanks to a genetically engineered line of technicolor zebrafish.
In the microscopic life that thrives around coral reefs, San Diego State University researchers have discovered an interplay between viruses and microbes that defies conventional wisdom. As the density of microbes rises in an ecosystem, the number of viruses infecting those microbes rises with it. It has generally been assumed that this growing population of viruses, in turn, kills more and more microbes, keeping the microbial population in check. It's a model known as "kill-the-winner" -- the winners being the blooming microbial cells and the killers being the viruses (mostly bacteria-killing viruses known as bacteriophages) that infect them.