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Category: genetics – Page 130

Denis Noble — Why The Last 80 Years of Biology was Wrong

We’re joined by Dr. Denis Noble, Professor Emeritus of Cardiovascular Physiology at the University of Oxford, and the father of ‘systems biology’. He is known for his groundbreaking creation of the first mathematical model of the heart’s electrical activity in the 1960s which radically transformed our understanding of the heart.

Dr. Noble’s contributions have revolutionized our understanding of cardiac function and the broader field of biology. His work continues to challenge long-standing biological concepts, including gene-centric views like Neo-Darwinism.

In this episode, Dr. Noble discusses his critiques of fundamental biological theories that have shaped science for over 80 years, such as the gene self-replication model and the Weissmann barrier. He advocates for a more holistic, systems-based approach to biology, where genes, cells, and their environments interact in complex networks rather than a one-way deterministic process.

We dive deep into Dr. Noble’s argument that biology needs to move beyond reductionist views, emphasizing that life is more than just the sum of its genetic code. He explains how AI struggles to replicate even simple biological systems, and how biology’s complexity suggests that life’s logic lies not in DNA alone but in the entire organism.

The conversation covers his thoughts on the flaws of Neo-Darwinism, the influence of environmental factors on evolution, and the future of biology as a field that recognizes the interaction between nature and nurture. We also explore the implications of his work for health and longevity, and how common perspectives on genetics might need rethinking.

All the topics we covered in the episode:

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Scientists decode key mutation in many cancers, pointing to expanded role of RNA in human gene expression

Inside every cell, inside every nucleus, your continued existence depends on an incredibly complicated dance. Proteins are constantly wrapping and unwrapping DNA, and even minor missteps can lead to cancer. A new study from the University of Chicago reveals a previously unknown part of this dance—one with significant implications for human health.

In the study, published Oct. 2 in Nature, a team of scientists led by UChicago Prof. Chuan He, in collaboration with University of Texas Health Science Center at San Antonio Prof. Mingjiang Xu, found that RNA plays a significant role in how DNA is packaged and stored in your cells, via a gene known as TET2. The paper is titled “RNA m5C oxidation by TET2 regulates chromatin state and leukaemogenesis.”

This pathway also appears to explain a long-standing puzzle about why so many cancers and other disorders involve TET2-related mutations—and suggests a set of new targets for treatments.

139,000 Neurons of Adult Fruit Fly Brain Mapped For The First Time

Unlocking the complexities of the fruit fly brain is a crucial step toward understanding the human brain. Fruit flies share many genetic similarities with humans, making them a valuable model organism for studying brain functions as well as diseases.

“An estimated 75% of human genes related to diseases have homologs in the fly genome,” Sebastian Seung, co-leader of the research team, told Interesting Engineering (IE).

“We’ve long known about the molecular similarities between fly and human brains. We have been slower to realize that there are also similarities at the circuit level, revealed by examining patterns of connectivity. We now know that fly circuits for olfaction, vision, and navigation have architectural similarities with mammalian circuits for the same functions,” Seung added.

Stanford Medicine study hints at ways to generate new neurons in old brains

The same technique could also be applied to studies of brain damage, Ruetz said. “Neural stem cells in the subventricular zone are also in the business of repairing brain tissue damage from stroke or traumatic brain injury.”

The glucose transporter connection “is a hopeful finding,” Brunet said. For one, it suggests not only the possibility of designing pharmaceutical or genetic therapies to turn on new neuron growth in old or injured brains, but also the possibility of developing simpler behavioral interventions, such as a low carbohydrate diet that might adjust the amount of glucose taken up by old neural stem cells.

The researchers found other provocative pathways worthy of follow-up studies. Genes relating to primary cilia, parts of some brain cells that play a critical role in sensing and processing signals such as growth factors and neurotransmitters, also are associated with neural stem cell activation. This finding reassured the team that their methodology was effective, partly because unrelated previous work had already discovered associations between cilia organization and neural stem cell function. It is also exciting because the association with the new leads about glucose transmission could point toward alternative avenues of treatment that might engage both pathways, Brunet said.

Filament structure found to activate and regulate CRISPR-Cas ‘protein scissors’

CRISPR-Cas systems help to protect bacteria from viruses. Several different types of CRISPR-Cas defense systems are found in bacteria, which differ in their composition and functions. Among them, the most studied proteins today are Cas9 and Cas12, also known as DNA or “gene scissors,” which have revolutionized the field of genome editing, enabling scientists to edit genomes and correct disease-causing mutations precisely.

Colossal Biosciences Launches $50 Million Foundation To Halt Extinction Crisis

The foundation hopes to prevent extinctions, and obtain the necessary biological material to safeguard genetic diversity.

Already backed by a confirmed $50 million in funding, its goal is to halt the extinction crisis through three key conservation focus points.

The Colossal Foundation’s first key…

Who ever said you can’t save a few species on the way to de-extincting a mammoth?

Antiviral innate immune memory in alveolar macrophages following SARS-CoV-2 infection ameliorates secondary influenza A virus disease

Pathogen encounter can result in epigenetic remodeling that shapes disease caused by heterologous pathogens.

The therapeutic potential of antigen-independent innate immune memory (IIM) is of particular relevance in the context of respiratory viruses with pandemic potential. Lercher et al. find that antiviral IIM in alveolar macrophages following SARS-CoV-2 infection ameliorates disease caused by a secondary unrelated pathogen, influenza A virus.

US scientist reveal mouth swab that can gauge your risk of death

U.S. researchers developed CheekAge, a tool that reliably estimates mortality risk.

Researchers in the United States have created a next-generation tool named CheekAge, which uses methylation patterns found in easily obtainable cheek cells.

In a groundbreaking discovery, the team has demonstrated that CheekAge can reliably estimate mortality risk, even when epigenetic data from different tissues are utilized for analysis.

Epigenetic markers are chemical changes to DNA that don’t alter the genetic code but can affect how genes work. Methylation is one such change, often linked to aging. Scientists use these patterns to create “age clocks” that estimate biological age, revealing how fast someone is aging.

New Tool Quantifies Cancer’s Ability to Shape-Shift

A powerful new analytical tool offers a closer look at how tumor cells “shape-shift” to become more aggressive and untreatable, as shown in a study from researchers at Weill Cornell Medicine and the New York Genome Center.

A tumor cell shape-shifts by changing its cell type or state, thus altering its basic pattern of activity and perhaps even its appearance. This changeability or “plasticity” is a characteristic of cancer that leads to diverse tumor-cell populations and ultimately the emergence of cell types enabling treatment resistance and metastatic spread.

The new tool, described Sept. 24 in a paper in Nature Genetics, can be used to quantify this plasticity in samples of tumor cells. The researchers demonstrated it with analyses of tumor samples from animal models and human patients, identifying, for example, a key transitional cell state in glioblastoma, the most common form of brain cancer.

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