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A groundbreaking study published in Nature Communications reveals how maternal and fetal genes, influenced by food availability, play a crucial role in the growth of a baby’s cerebral cortex, linking higher birth weight to an enlarged brain area. This research highlights the significant impact of genetics and environment on early brain development.

For the survival of life on Earth, the process where plants perform photosynthesis to generate oxygen and chemical energy using sunlight is crucial. Scientists from Göttingen and Hannover have now achieved a breakthrough by creating a high-resolution 3D visualization of the chloroplasts’ copying mechanism, the RNA polymerase PEP, for the first time. This intricate structure offers fresh perspectives on the operation and evolutionary history of this vital cellular apparatus, instrumental in interpreting the genetic blueprints for proteins involved in photosynthesis.

Without photosynthesis, there would be no air to breathe – it is the basis of all life on Earth. This complex process allows plants to convert carbon dioxide and water into chemical energy and oxygen using light energy from the sun. The conversion takes place in the chloroplasts, the heart of photosynthesis. Chloroplasts developed in the course of evolution when the ancestors of today’s plant cells absorbed a photosynthetic cyanobacterium. Over time, the bacterium became increasingly dependent on its “host cell”, but maintained some significant functions such as photosynthesis and parts of the bacterial genome. The chloroplast therefore still has its own DNA, which contains the blueprints for crucial proteins of the “photosynthesis machinery”

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In a recent review published in the Journal of Human Genetics, a group of authors explored the potential of deep learning (DL), particularly convolutional neural networks (CNNs), in enhancing predictive modeling for omics data analysis, addressing challenges and future research directions.

Study: Advances in AI and machine learning for predictive medicine. Image Credit: NicoElNino/Shutterstock.com.

Charles Darwin described evolution as “descent with modification.” Genetic information in the form of DNA sequences is copied and passed down from one generation to the next. But this process must also be somewhat flexible, allowing slight variations of genes to arise over time and introduce new traits into the population.

But how did all of this begin? In the origins of life, long before cells and proteins and DNA, could a similar sort of evolution have taken place on a simpler scale? Scientists in the 1960s, including Salk Fellow Leslie Orgel, proposed that life began with the “RNA World,” a hypothetical era in which small, stringy RNA molecules ruled the early Earth and established the dynamics of Darwinian evolution.

Continue reading “Modeling the origins of life: New evidence for an ‘RNA World’” »

Myeloid cells are a population of cells classified to denote a specific lineage. “Myeloid” specifically refers to granulocytes and monocytes generated from the bone marrow. Many cells under this term share common progenitors from which they derive including, macrophages, neutrophils, basophils, and eosinophils. In the context of cancer, many of these cells become ‘pro-tumorigenic’. More specifically, they suppress the immune system to allow the tumor to proliferate and progress. Each myeloid cell type is associated with antitumor immune suppression. Myeloid cells suppress antitumor immune activity by blocking T cell activation, aid in angiogenesis (blood vessel formation) to increase metastasis, and producing cytokines or proteins that activate suppressive activity in other cells. Unfortunately, myeloid cells make up a major percentage within the tumor microenvironment, so targeting these cells is crucial. Many researchers are currently working on different ways to target these cell populations.

A recent article in Nature by Dr. Miriam Merad and her team demonstrated how protein signaling drives pro-tumor myeloid cell generation. Merad is a physician scientist, Director of the Precision Immunology Institute at Mount Sinai School of Medicine in New York, and Director of the Mount Sinai Human Immune Monitoring Center (HIMC). While her work focuses on targeting myeloid cells (particularly macrophages) to lower their suppressive phenotype and improve cancer treatment, her current publication identifies specific drivers of immunosuppressive myeloid states, previously undefined.

Merad and her team used advanced single cell sequencing to analyze non-small cell lung cancer (NSCLC) lesions from both humans and mice. Single cell sequencing is commonly used to identified up-and downregulated genes in a variety of cell types. By sequencing the tumor lesions the team discovered that interleukin 4 (IL-4) was a predictive driver of macrophages that infiltrated the tumor. Researchers used various genetically modified mouse models to conclude that the IL-4 receptor is necessary for tumor progression. Interestingly, they concluded that deletion of the IL-4 receptor in the progenitor phase reduced tumor growth compared to IL-4 deletion in mature macrophages which had little effect.

As a therapy for vision impairment resulting from inherited retinal degeneration, the mRNA would instruct cells in the retina, which are impaired because of a genetic mutation, to manufacture the proteins needed for sight. Inherited retinal degeneration, commonly abbreviated to IRD, encompasses a group of disorders of varying severity and prevalence that affect one out of every few thousand people worldwide.

An example of a genetic pulmonary condition is cystic fibrosis, a progressive disorder that results in persistent lung infection and affects 30,000 people in the U.S., with about 1,000 new cases identified every year. One faulty gene—the cystic fibrosis transmembrane conductance regulator, or CFTR—causes the disease, which is characterized by lung dehydration and mucus buildup that blocks the airway.

The thiophene-based LNP study, which involved mice and non-human primates, stems from a $3.2 million grant from the National Eye Institute. The grant’s purpose is addressing limitations associated with the current primary means of delivery for gene editing: adeno-associated virus, or AAV.

Cancer cells are characterized by their aggressiveness: they grow rapidly and spread to other parts of the body. To enable this, numerous mechanisms come into play, and one of them involves a protein called MYC, which activates certain genes on the cancer cell’s DNA strand, causing the cancer cell to grow and divide.

The MYC protein is also present in healthy individuals, where it plays a crucial role in regulating many cell functions.

“When cancer occurs, it is due to an accumulation of mutations in our DNA, often resulting in the overactivation of the MYC protein. Therefore, this protein plays a crucial role in most cancer forms,” says Rasmus Siersbæk, head of research at the Department of Biochemistry and Molecular Biology, University of Southern Denmark.

Every time a cell divides, its DNA is duplicated so that the two daughter cells have the same genetic material as their parent. This means that, millions of times a day, a biochemical wonder takes place in the body: the copying of the DNA molecule. It is a high-precision job carried out by specific proteins and includes systems to protect against potential errors that could lead to diseases such as cancer.

One of these anti-failure systems has just been discovered by researchers in the DNA Replication Group at the Spanish National Cancer Research Centre (CNIO), led by Juan Méndez. It is based on a protein that ensures that DNA is copied only once, as it should be, and not twice or more.

The work is published in The EMBO Journal.