A long-standing assumption about evolution is being challenged by new research showing that vastly different species can rely on the same genetic pathways to develop similar traits.
Category: genetics – Page 6
Genetic parallelism underpins convergent mimicry coloration in Lepidoptera across 120 million years of evolution
The repeated evolution of similar phenotypes, or convergent evolution, is widespread in nature, but there are few studies investigating the genetic mechanisms across wide evolutionary timescales. This study examines convergent wing pattern evolution across highly divergent Lepidopteran lineages and reports parallel genetic reuse, indicating strong constraints and high predictability in evolutionary outcomes.
An ultrasound-scanning in vivo light source
Beautifully executed paper on putting mechanoluminescent nanoparticles into blood circulation of mice which express optogenetic channels. Focused ultrasound can then trigger targeted light emission and control of neural activity in the brain and elsewhere.
A deep-tissue light source made from mechanoluminescent transducers stimulated by focused ultrasound enables wide imaging of live animal vasculature, and modulation of neuronal activity and behaviour.
A simple filter swap could advance marine eDNA biomonitoring
Researchers at Aarhus University have demonstrated that a simple adjustment to water filtration methods can dramatically improve the detection of marine animal DNA when using advanced, PCR-free sequencing. This methodological optimization could help clear a major bottleneck in aquatic biomonitoring and marine conservation efforts. The study is published in Metabarcoding and Metagenomics.
Over the past two decades, environmental DNA (eDNA) analysis has become a crucial tool for monitoring aquatic ecosystems. The most common method, metabarcoding, relies on PCR amplification of a smaller genetic region to identify specific taxa. However, PCR can lead to “significant taxonomic bias” because it often amplifies the DNA of different organisms unequally, making quantitative estimates difficult.
To avoid this, scientists have increasingly explored “shotgun sequencing”—a broad approach that sequences the DNA in a sample much more broadly—across the entire tree of life and across the genome.
Cell-by-cell analysis uncovers 345 risk genes across six neuropsychiatric disorders
The emergence of neuropsychiatric disorders, conditions that affect various brain functions and behaviors, is known to be driven by an intricate combination of factors. These can include both a genetic predisposition and exposure to traumatic events or other external circumstances.
Over the past decades, many neuroscience studies have tried to shed light on the origins of different mental health disorders. However, the biological, cellular and molecular mechanisms underpinning these disorders have not yet been clearly elucidated.
Researchers at Peking University Sixth Hospital and Peking University Institute of Mental Health recently analyzed genetic data collected from patients diagnosed with six different neuropsychiatric disorders, to better delineate the genes and cell types that contribute to their emergence. Their paper, published in Molecular Psychiatry, identifies 345 genes expressed in different types of cells that were linked to an increased risk of developing these disorders.
Swine reporter model for preclinical evaluation and characterization of gene delivery vectors
Pigs which express tdTomato upon Cre or CRISPR editing of a genetic cassette inserted into their genome. (Pig analogue of Ai9 mice). This model system will aid translational preclinical studies for gene editing therapies.
A “turn-on” swine reporter model is developed to characterize local and systemic delivery of gene editors in vivo using viral or non-viral vectors. This adds the functionality of a reporter to preclinical gene delivery research in a large animal model that is more broadly accessible than nonhuman primates.
ALDH1L2 regulates reactive oxygen species and acinar-to-ductal metaplasia in the pancreas
Role of NADPH enzymes in pancreatic cancer.
Pancreas repair following injury involves reversible acinar-to-ductal metaplasia (ADM) and oncogenic KRAS mutations can progress ADM to pancreatic intraepithelial neoplasia (PanIN) and pancreatic ductal adenocarcinoma (PDAC) but, the metabolic alterations in these precancerous lesions are not established.
In 2 studies published in Nature Metabolism, researchers demonstrate decline in NADPH producing enzymes that reduce oxidative stress and protect the pancreatic cells.
In one study, the authors show aldehyde dehydrogenase 1 family member L2 (ALDH1L2), an NADPH-producing mitochondrial enzyme expression level decreases progressively during ADM and is completely absent in pancreatic ductal cells. ALDH1L2 loss elevates ROS and promotes ADM in a model of pancreatitis and accelerates tumor progression in models of pancreatic cancer.
In the 2nd study, the authors show NRF2-target genes are significantly induced in ADM. Among these, genes encoding NADPH-producing enzymes glucose-6-phosphate dehydrogenase (G6PD) and malic enzyme 1 (ME1), which participate in the regulation of oxidative stress.
In mouse models of pancreatic tumorigenesis, G6PD deficiency or Me1 loss increases reactive oxygen species and lipid peroxidation, which is accompanied by accelerated formation of ADM and PanIN lesions. The authors also show that Me1 loss, but not G6PD deficiency, promotes faster PDAC progression. sciencenewshighlights Science Mission https://www.nature.com/articles/s42255-026-01496-x https://sciencemission.com/NADPH-producing-enzymes https://sciencemission.com/ALDH1L2-regulates-reactive-oxygen-species
AI tackles one of math’s most brutal problems: Inverse PDEs
Penn Engineers have developed a new way to use AI to solve inverse partial differential equations (PDEs), a particularly challenging class of mathematical problems with broad implications for understanding the natural world.
The advance, which the researchers call “Mollifier Layers,” could benefit fields as varied as genetics and weather forecasting, because inverse PDEs help scientists work backward from observable patterns to infer the hidden dynamics that produced them.
“Solving an inverse problem is like looking at ripples in a pond and working backward to figure out where the pebble fell,” says Vivek Shenoy, Eduardo D. Glandt President’s Distinguished Professor in Materials Science and Engineering (MSE) and senior author of a study published in Transactions on Machine Learning Research (TMLR), which will be presented at the Conference on Neural Information Processing Systems (NeurIPS 2026). “You can see the effects clearly, but the real challenge is inferring the hidden cause.”
Abstract: SLC26A4-gene mutations are a frequent cause of hereditary HearingLoss
SLC26A4-gene mutations are a frequent cause of hereditary HearingLoss.
https://doi.org/10.1172/JCI193812 Here, Tsai et al. report that targeted AAV delivery to the endolymphatic sac and cochlear lateral wall restores auditory physiology and ameliorates cochlear pathology in a mouse model of Slc26a4-related deafness. Pendred syndrome DFNB4.
The image shows an AAV-GFP–transduced spiral prominence, a structure within the cochlear lateral wall. GFP (green) marks successfully transduced cells, phalloidin-568 (red) labels the actin cytoskeleton, and DAPI (blue) stains nuclei, highlighting efficient gene transfer to inner ear tissues essential for auditory function.
Address correspondence to: Chen-Chi Wu, Department of Otolaryngology, National Taiwan University Hospital, No. 1, Changde St., Zhongzheng Dist., Taipei City 100,229, Taiwan. Phone: 886.2.2312.3456; Email: [email protected]. Or to: Yen-Fu Cheng, Department of Medical Research, Taipei Veterans General Hospital, No. 201, Sec. 2, Shipai Rd., Beitou District, Taipei City 11,217, Taiwan. Phone: 886.2.2875.7642; Email: [email protected].
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1Institute of Brain Science, College of Medicine, National Yang Ming Chiao Tung University, Taipei, Taiwan.