Lifeboat Foundation

Cells in the human body contain power-generating mitochondria, each with their own mtDNA—a unique set of genetic instructions entirely separate from the cell’s nuclear DNA that mitochondria use to create life-giving energy. When mtDNA remains where it belongs (inside of mitochondria), it sustains both mitochondrial and cellular health—but when it goes where it doesn’t belong, it can initiate an immune response that promotes inflammation.

Now, Salk scientists and collaborators at UC San Diego have discovered a novel mechanism used to remove improperly functioning mtDNA from inside to outside the mitochondria. When this happens, the mtDNA gets flagged as foreign DNA and activates a cellular pathway normally used to promote inflammation to rid the cell of pathogens, like viruses.

The findings, published in Nature Cell Biology, offer many new targets for therapeutics to disrupt the inflammatory pathway and therefore mitigate inflammation during aging and diseases, like lupus or rheumatoid arthritis.

A technique can determine for the first time how frequently, and exactly where, a molecular event called “backtracking” occurs throughout the genetic material (genome) of any species, a new study shows.

Published online February 9 in Molecular Cell, the study results support the theory that backtracking represents a widespread form of gene regulation, which influences thousands of human genes, including many involved in basic life processes like cell division and development in the womb.

Led by researchers from NYU Grossman School of Medicine, the work revolves around genes, the stretches of DNA molecular “letters” arranged in a certain order (sequence) to encode the blueprints for most organisms. In both humans and bacteria, the first step in a gene’s expression, transcription, proceeds as a protein “machine” called RNA polymerase II ticks down the DNA chain, reading genetic instructions in one direction.

In a new Nature Communications study, researchers have explored the construction of genetic circuits on single DNA molecules, demonstrating localized protein synthesis as a guiding principle for dissipative nanodevices, offering insights into artificial cell design and nanobiotechnology applications.

The term “genetic circuit” is a metaphorical description of the complex network of genetic elements (such as genes, promoters, and regulatory proteins) within a cell that interact to control gene expression and cellular functions.

In the realm of artificial cell design, scientists aim to replicate and engineer these genetic circuits to create functional, self-contained units. These circuits act as the molecular machinery responsible for orchestrating cellular processes by precisely regulating the production of proteins and other molecules.

While combing through the human genome in 2007, computational geneticist Pardis Sabeti made a discovery that would transform her research career. As a then-postdoctoral fellow at the Broad Institute of MIT and Harvard, Sabeti discovered potential evidence that some unknown mutation in a gene called LARGE1 had a beneficial effect in the Nigerian population.

Other scientists had discovered that this gene was critical for the Lassa virus to enter cells. Sabeti wondered whether a mutation in LARGE1 might prevent Lassa fever—an infection that is caused by the Lassa virus, is endemic in West Africa, and can be deadly in some people while only mild in others.

To find out, Sabeti decided later in 2007, as a new faculty member at Harvard University, that one of the first projects her new lab at the Broad would take on would be a genome-wide association study (GWAS) of Lassa susceptibility. She reached out to her collaborator Christian Happi, now the Director of the African Center of Excellence for Genomics of Infectious Diseases (ACEGID) at Redeemer’s University in Nigeria, and together they launched the study.

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A study at the University of Cologne’s CECAD Cluster of Excellence in Aging Research has identified a protein complex that is activated by defects in the spliceosome, the molecular scissors that process genetic information. Future research could lead to new therapeutic approaches to treat diseases caused by faulty splicing.

The genetic material, in the form of DNA, contains the information that is crucial for the correct functioning of every human and animal cell. From this information repository, RNA, an intermediate between DNA and protein, the functional unit of the cell, is generated. During this process, the genetic information must be tailored for specific cell functions. Information that is not needed (introns) is cut out of the RNA and the important components for proteins (exons) are preserved.

A team of researchers led by Professor Dr. Mirka Uhlirova at the University of Cologne’s CECAD Cluster of Excellence in Aging Research has now discovered that if the processing of this information no longer works properly, a protein complex (C/EBP heterodimer) is activated and directs the cell towards a dormant state, known as cellular senescence. The results appear under the title “Xrp1 governs the stress response program to spliceosome dysfunction” in Nucleic Acids Research.

Scientists have been making nanoparticles out of DNA strands for two decades, manipulating the bonds that maintain DNA’s double-helical shape to sculpt self-assembling structures that could someday have jaw-dropping medical applications.

The study of DNA nanoparticles, however, has focused mostly on their architecture, turning the genetic code of life into components for fabricating minuscule robots. A pair of Iowa State University researchers in the genetics, development, and cell biology department—professor Eric Henderson and recent doctoral graduate Chang-Yong Oh—hope to change that by showing nanoscale materials made of DNA can convey their built-in genetic instructions.

“So far, most people have been exploring DNA nanoparticles from an engineering perspective. Little attention has been paid to the information held in those DNA strands,” Oh said.

An international team of researchers has identified the genetic basis and biological processes that influence cancer risk related to alterations in the number of immune cells present in the blood. This is a significant advance in understanding how the immune system can prevent the appearance of tumors.

The study, led by researchers from the Institut Català d’Oncologia (ICO), the Bellvitge Biomedical Research Institute (IDIBELL), the Germans Trias i Pujol Research Institute (IGTP), and the Translational Genomics Research Institute in the United States, has been published in the journal Genome Medicine and represents a significant step towards a better understanding of how alterations in the immune system facilitate the onset of cancer.

The immune system is responsible for maintaining the integrity and function of the body by continuously protecting us from exogenous attacks, such as viruses and endogenous attacks, in this case, cancer. This gives it a central role in inhibiting carcinogenesis, and its disruption may increase the risk of cancer by allowing malignant cells to proliferate.

Norovirus, a highly infectious virus that is the leading cause of diarrhea and vomiting in the U.S., has no approved therapeutics or vaccines to prevent its miserable effects. This is partly due to a lack of reliable animal models to study norovirus infection and predict how effective interventions would be in people. To solve this, NIAID scientists have developed an animal model to study human norovirus infection that could help facilitate the development of new vaccines and therapeutics to treat norovirus infection. Findings from this research were published Feb. 6 in Nature Microbiology.

Human norovirus causes illness in tens of millions of people in the U.S. each year and, in some cases, can result in hospitalization and even death. It is easily spread when people ingest foods, drinks or particles from surfaces contaminated by virus from the stool or vomit of an infected individual. Noroviruses are genetically diverse, with different genogroups—groups characterized by genetic similarity—of the virus infecting different species of animals. Several genogroups of noroviruses infect people without similarly infecting animals. This has led to difficulties in establishing an animal model for human norovirus infection.

Following up on earlier evidence that rhesus macaque monkeys could develop norovirus infections, a team of researchers led by scientists at NIAID’s Vaccine Research Center set out to determine whether macaques could serve as an effective animal model for the human disease. The macaques were challenged with several genotypes of human noroviruses at once. Throughout the experiment, the animals were kept in biocontainment, and their health and behavior were carefully monitored. Levels of virus in the animals’ stool were measured, and antibodies against norovirus in the animals’ blood serum were analyzed. The researchers found that the macaques were susceptible to viral infection with at least two genotypes of norovirus, with similar antibody responses, shedding of virus in stool, and pathology as in human norovirus infection. Notably, the infections in the animals did not result in clinical symptoms, such as diarrhea and vomiting.