Researchers discover Hand2 gene plays key role in providing positional information for limb regeneration in axolotls. The discovery provides new insights into how cells 'remember' their position and switch on signals to regenerate structures correctly.
Researchers identified a molecular mechanism that controls embryonic diapause in humans, allowing cells to temporarily slow down development. This dormant state is characterized by reduced cell division and slower development, and can be reversed when the mTOR pathway is reactivated.
Researchers at IMBA discovered a parent-of-origin effect in nematodes, suggesting the first step in genomic imprinting's evolution. This finding provides insight into how imprinting arose independently in mammals and plants over 100 million years ago.
A new organoid model replicates the dopaminergic system's structure, connectivity, and functionality, shedding light on its intricate functionality and potential implications for Parkinson’s disease. The model also uncovers the enduring effects of chronic cocaine exposure on the dopaminergic circuit, even after withdrawal.
Researchers create a new, multi-chamber organoid model of the human heart, enabling them to advance screening platforms for drug development, toxicology studies, and understanding heart development. The model reveals intricate communication between chambers and provides insight into early heart development.
Researchers at IMBA Institute of Molecular Biotechnology have identified a new gene, Daam1, that plays an essential role in switching on the development of secretory cells in the intestine. The finding opens new perspectives in cancer research.
Researchers developed a technique called CHOOSE that allows them to test the effect of multiple mutations in parallel and at a single-cell level within human brain organoids. The study identified critical transcriptional changes regulated through common networks, or GRNs, and found that some cell types are more susceptible to autism mu...
Researchers from IMBA identify a family of virus-like transposons called Mavericks that facilitate horizontal gene transfer (HGT) between reproductively isolated worm species. The study reveals the role of Mavericks in overcoming the species barrier, with potential applications in pathogen control and genomic innovation.
A study by IMBA researchers links muscle degeneration to a deficiency in the enzyme PCYT2, essential for lipid synthesis. PCYT2 depletion affects mitochondrial function and muscle energetics, highlighting the importance of lipid balance in muscle health.
Researchers identified the molecular mechanism underlying Weiss-Kruszka syndrome, a rare neurodevelopmental disorder characterized by craniofacial anomalies and autistic features. The study reveals that the ZFP462 gene mutation leads to a failure to safeguard neural lineage specification during early embryonic development.
The HUSH complex is involved in normal brain development, neuronal individuality, and connectivity. The complex also regulates repetitive-like gene clusters, including protocadherin gene clusters, which are essential for neuron-to-neuron interactions.
Researchers at IMBA found that Kipferl helps distribute Rhino to piRNA clusters, avoiding sequestration to Satellite arrays. This control mechanism ensures the effective silencing of jumping genes and maintains genome stability.
A newly identified link between chronic pain and lung cancer in mice suggests that old drugs such as clonidine, capsaicin, and fluphenazine may offer new treatments for chronic pain. The study found that blocking the BH4 pathway reduced pain sensitivity and decreased tumor growth in mouse models of KRAS-driven lung cancer.
The Gerlich Group at IMBA found that histone acetylation establishes a sharp surface boundary on chromosomes, resisting microtubule perforation. Chromatin phase separation and DNA looping by condensin cooperates to build mitotic chromosomes with unique physical properties.
Researchers using 'blastoids' - in vitro models of the blastocyst - discovered that early embryonic signals induce placental development and prepare the uterus. The findings may contribute to a better understanding of human fertility and potentially improve IVF procedures, fertility drugs, and contraceptives.
A molecular switch, p57, enables stomach stem cells to change allegiance from normal digestion to injury response, potentially leading to new treatments for gastric pathologies. The study's findings suggest that p57 is a key regulator of reserve stem cell state in gastric chief cells.
Breakthrough research reveals Tuberous Sclerosis Complex arises from human-specific progenitor cells, explaining its pathology. Human-derived cerebral organoid models shed light on complex brain development and potential mechanisms for other diseases.
Researchers have discovered molecules that could be candidates for contraceptives or fertility enhancers using human blastoid models. These models also show promise in improving the self-organization of stem cells during IVF procedures.
Researchers identified two lectins, Clec4g and CD209c, that strongly bind to the SARS-CoV-2 Spike protein, blocking viral entry into cells. These findings hold promise for developing robust therapeutic interventions against circulating variants.
A team of researchers developed a laboratory system to dissect the pre-cancerous steps that remained undetected until present. They found that mutant cells create a hostile environment for neighboring non-mutant cells and deregulate the normal stem cell niche in mouse intestinal tissue.
Researchers developed a method called SARSeq that enables large groups to be tested for SARS-CoV-2 with the same sensitivity as regular PCR tests. The method processes up to 36,000 samples in less than 48 hours and is highly specific and scalable.
Researchers developed cardioids, human self-organizing cardiac organoids that recapitulate heart chamber formation and function. The model reveals how signaling and transcription factors control cardioid chamber formation and triggers an in vivo-like accumulation of extracellular matrix proteins after injury.
Using human brain organoid models, researchers demonstrate various viruses cause microcephaly through different mechanisms. ZIKV and HSV-1 infections impair neuroepithelial identity and attenuate Type I interferon responses.
Researchers have identified the SFiNX complex as a key player in silencing transposons through a DNA-RNA crosstalk mechanism. This interaction enables other domains within the complex or co-recruited silencing effectors to establish heterochromatin, leading to gene expression regulation.
Researchers identified five novel toxin-antidote pairs in nematode species Caenorhabditis tropicalis and C. briggsae. The study found that these elements can delay reproduction or kill non-carriers, causing defects in over 70% of progeny from a single cross.
A study found that the thymus produces specialized cells called 'Tregs' during pregnancy to deal with physiological changes. RANK, a receptor expressed in the thymus epithelium, is the key molecule behind this mechanism.
Researchers developed a new technique, CRISPR-LICHT, allowing for the analysis of hundreds of genes in human tissue using cerebral organoids. The method identified a specific mechanism controlling brain size and pinpointed microcephaly genes, shedding light on a genetic disorder.
Scientists have developed a method to create high-resolution maps of contact points between replicated chromosomes, providing insights into the molecular machinery regulating DNA conformation and repair. This breakthrough could shed light on the mechanics underlying genome transport during cell division.
Researchers found that Casein Kinase-1 regulates the Wnt signaling pathway at the plasma membrane, triggering the activation of RNF43. This new understanding could lead to a novel approach for reining the Wnt pathway in cancer cells, potentially reviving the tumor suppressor function of RNF43.
Researchers found that Brat tumors in Drosophila are highly oxidative, with increased oxygen consumption rates compared to normal brains. Oxidative metabolism plays a key role in tumor cell immortalization, driven by mitochondrial fusion and increased efficiency in oxidative phosphorylation.
A recent study published in Nature reveals that the protein Ki-67 plays a crucial role in excluding large cytoplasmic components from the nucleus before nuclear envelope reassembly. This exclusion process is essential for maintaining cellular compartmentalization and preventing premature translation of immature RNAs.
Researchers identify ALK as a candidate gene for thinness by studying Estonian population cohort and finding it is involved in regulating energy expenditure and sympathetic tone. ALK deficient mice exhibit reduced fat mass and protected against diet-induced obesity.