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Category: genetics – Page 166

Chromatin structures and transcriptional networks are known to specify cell identity during development which directs cells into metaphorical valleys in the Waddington landscape. Cells must retain their identity through the preservation of epigenetic information and a state of low Shannon entropy for the maintenance of optimal function. Yeast studies in the 1990s have reported that a loss of epigenetic information compared to genetics can cause aging. Few other studies also confirmed that epigenetic changes are not just a biomarker but a cause of aging in yeasts.

Epigenetic changes associated with aging include changes in DNA methylation (DNAme) patterns, H3K27me3, H3K9me3, and H3K9me3. Many epigenetic changes have been observed to follow a specific pattern. However, the reason for changes in the mammalian epigenome is not yet known. A few clues can be obtained from yeast, where DSB is a significant factor whose repair requires epigenetic regulators Esa1, Gcn5, Rpd3, Hst1, and Sir2. As per the ‘‘RCM’’ hypothesis and ‘Information Theory of Aging’’, aging in eukaryotes occurs due to the loss of epigenetic information and transcriptional networks in response to cellular damage such as a crash injury or a DSB.

A new study in the journal Cell aimed to determine whether epigenetic changes are a cause of mammalian aging.

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A new study led by scientists at Rutgers University has uncovered new insights into the underlying brain mechanisms of autism spectrum disorder.

Autism Spectrum Disorder (ASD) is a complex developmental disorder that affects how a person communicates and interacts with others. It is characterized by difficulty with social communication and interaction, as well as repetitive behaviors and interests. ASD can range from mild to severe, and individuals with ASD may have a wide range of abilities and challenges. It is a spectrum disorder because the symptoms and characteristics of ASD can vary widely from person to person. Some people with ASD are highly skilled in certain areas, such as music or math, while others may have significant learning disabilities.

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Bats (Mammalia: Chiroptera) serve as natural reservoirs for many zoonotic pathogens worldwide, including vector-borne pathogens. However, bat-associated parasitic arthropods and their microbiota are thus far not thoroughly described in many regions across the globe, nor is their role in the spillover of pathogens to other vertebrate species well understood. Basic epidemiological research is needed to disentangle the complex ecological interactions among bats, their specific ectoparasites and microorganisms they harbor. Some countries, such as Ukraine, are particularly data-deficient in this respect as the ectoparasitic fauna is poorly documented there and has never been screened for the presence of medically important microorganisms. Therefore, the aims of this study were to provide first data on this topic.

A total of 239 arthropod specimens were collected from bats. They belonged to several major groups of external parasites, including soft ticks, fleas, and nycteribiid flies from six chiropteran species in Northeastern Ukraine. The ectoparasites were individually screened for the presence of DNA of Rickettsia spp., Anaplasma/Ehrlichia spp., Bartonella spp., Borrelia spp., and Babesia spp. with conventional PCRs. Positive samples were amplified at several loci, sequenced for species identification, and subjected to phylogenetic analysis.

Rickettsia DNA was detected exclusively in specimens of the soft tick, Carios vespertilionis (7 out of 43 or 16.3%). Sequencing and phylogenetic analysis revealed high similarity to sequences from Rickettsia parkeri and several other Rickettsia species. Bacteria from the family Anaplasma taceae were detected in all groups of the ectoparasites (51%, 122/239 samples), belonging to the genera Anaplasma, Ehrlichia, and Wolbachia. The detection of Bartonella spp. was successful only in fleas (Nycteridopsylla eusarca) and bat flies (Nycteribia koleantii, N. pedicularia), representing 12.1% (29÷239) of the collected ectoparasites. No DNA of Babesia or Borrelia species was identified in the samples.

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Excessive fear is a hallmark of anxiety disorders, a major cause of disease burden worldwide. Substantial evidence supports a role of prefrontal cortex-amygdala circuits in the regulation of fear and anxiety, but the molecular mechanisms that regulate their activity remain poorly understood. Here, we show that downregulation of the histone methyltransferase PRDM2 in the dorsomedial prefrontal cortex enhances fear expression by modulating fear memory consolidation. We further show that Prdm2 knock-down (KD) in neurons that project from the dorsomedial prefrontal cortex to the basolateral amygdala (dmPFC-BLA) promotes increased fear expression. Prdm2 KD in the dmPFC-BLA circuit also resulted in increased expression of genes involved in synaptogenesis, suggesting that Prdm2 KD modulates consolidation of conditioned fear by modifying synaptic strength at dmPFC-BLA projection targets.

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When genes are activated and expressed, they show patterns in cells that are similar in type and function across tissues and organs. Discovering these patterns improves our understanding of cells—which has implications for unveiling disease mechanisms.

The advent of spatial transcriptomics technologies has allowed researchers to observe gene expression in their spatial context across entire tissue samples. But new computational methods are needed to make sense of this data and help identify and understand these .

A research team led by Jian Ma, the Ray and Stephanie Lane Professor of Computational Biology in Carnegie Mellon University’s School of Computer Science, has developed a machine learning tool to fill this gap. Their paper on the method, called SPICEMIX, appeared as the cover story in the most recent issue of Nature Genetics.

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The rebooting came in the form of a gene therapy involving three genes that instruct cells to reprogram themselves—in the case of the mice, the instructions guided the cells to restart the epigenetic changes that defined their identity as, for example, kidney and skin cells, two cell types that are prone to the effects of aging. These genes came from the suite of so-called Yamanaka stem cells factors—a set of four genes that Nobel scientist Shinya Yamanaka in 2006 discovered can turn back the clock on adult cells to their embryonic, stem cell state so they can start their development, or differentiation process, all over again. Sinclair didn’t want to completely erase the cells’ epigenetic history, just reboot it enough to reset the epigenetic instructions. Using three of the four factors turned back the clock about 57%, enough to make the mice youthful again.

“We’re not making stem cells, but turning back the clock so they can regain their identity,” says Sinclair. “I’ve been really surprised by how universally it works. We haven’t found a cell type yet that we can’t age forward and backward.”

Rejuvenating cells in mice is one thing, but will the process work in humans? That’s Sinclair’s next step, and his team is already testing the system in non-human primates. The researchers are attaching a biological switch that would allow them to turn the clock on and off by tying the activation of the reprogramming genes to an antibiotic, doxycycline. Giving the animals doxycycline would start reversing the clock, and stopping the drug would halt the process. Sinclair is currently lab-testing the system with human neurons, skin, and fibroblast cells, which contribute to connective tissue.

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San Diego-based biotech startup Rejuvenate Bio is making a major claim that’ll likely draw heated scrutiny from the scientific community: that its technology was able to significantly extend the lives of elderly mice.

According to a yet-to-be-peer-reviewed paper, scientists at the company say an injection that reprograms genes in the bodies of senior mice effectively doubled their remaining life span, MIT Technology Review reports.

In tests, the company found that treated mice lived on for another 18 weeks on average. Those who were not treated in a control group only lived for another nine weeks. Overall, they say, the gene hacked mice lived roughly seven percent longer overall.

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