İzzet O.

Good morning mito-folks, don't miss this rich selection of papers related to #mitochondrialmedicine presorted by @Bims_BiomedNews biomed.news/bims-mitmed/20… A perinatal approach for unravelling mitochondrial function in preeclampsia and fetal growth restriction

The backlash against artificial intelligence is growing. What do you think about its impact on science? go.nature.com/4dBGkNM

T cells initiate inhibitory #PD1 signaling at microvillar close contacts with target cells, limiting T cell receptor signaling duration and T cell activation. @DrEdJenks @KlenermanLab Learn more in Science #Immunology: scim.ag/437cuvB

Endosome maturation is orchestrated by inside-out proton signaling through a Na+/H+ exchanger and pH-dependent Rab GTPase cycling | Nature Communications nature.com/articles/s4146…

43 years ago, Michael Jackson stepped onto the stage in that fedora and gave the world the moonwalk for the very first time 🕺✨ A legendary Billie Jean performance that still feels untouchable today 🔥🔥

Large-scale metaproteomics of human gut microbiota reveals microbial functions in metabolic diseases and aging dlvr.it/TSQQS3

Coğrafyanın içindeki fizik

Immune cells regulate circulating adipocyte extracellular vesicle levels in response to metabolic shifts dlvr.it/TSPqjY

Preservation of chondrocyte microspheroids by local sustained hydrogen supply improves osteoarthritic cartilage repair dlvr.it/TSQlRK

Kibrit çöpü, kulak çöpü… nedir bu çöp?

Golgi–Mitochondria Contact Sites: The Hidden Lipid–Stress Interface Mitochondria are no longer “stand-alone powerhouses.” They operate as networked organelles, physically coupled to the ER, Golgi, lysosomes, lipid droplets, and plasma membrane through membrane contact sites. One emerging axis is especially underexplored: Golgi–mitochondria communication. Recent reviews and mechanistic studies suggest that Golgi-derived membranes and lipids may participate in mitochondrial remodeling, respiratory adaptation, and stress signaling—not simply through vesicular trafficking, but via direct or three-way ER–Golgi–mitochondria contact platforms. The Golgi contact-site review The Fast and the Furious: Golgi Contact Sites highlighted Golgi–mitochondria contacts as one of the most experimentally supported new Golgi contact interfaces, especially in lipid exchange and mitochondrial dynamics. The key concept: Golgi-derived PI4P/lipid-enriched vesicles may be recruited near ER–mitochondria contact sites, creating a three-organelle signaling hub that coordinates lipid supply, mitochondrial fission, and metabolic adaptation. This shifts the Golgi from “post-ER cargo station” to an active regulator of mitochondrial state. A second layer comes from COPI biology. COPI is classically known for Golgi–ER retrograde trafficking, but a 2023 Cell Reports study showed that COPI disruption reduces mitochondria–ER contact sites, impairs Ca²⁺ handling, increases mitophagy, decreases respiratory capacity, and accelerates axonal degeneration. Restoring MERCS partially rescued mitochondrial and neuronal phenotypes. This suggests a causal chain: Golgi–ER traffic → MERCS integrity → mitochondrial Ca²⁺/respiration → cell survival For aging, neurodegeneration, cancer metabolism, and fibrosis, this is a rich hypothesis space. Golgi–mitochondria/MERCS dysfunction could act as a hidden “organelle logistics failure” linking lipid imbalance, mitochondrial fragmentation, impaired respiration, and chronic stress signaling. The field now needs better tools: split-FP proximity reporters, EM tomography, proximity labeling, lipidomics, and perturbation screens to distinguish true contact-site biology from nearby organelle crowding. A 2023 methods review provides a useful technical roadmap for studying membrane contact sites. Working hypothesis: Golgi–mitochondria contact is not a minor cell-biology curiosity. It may be a tunable metabolic control node—where lipid trafficking, mitochondrial dynamics, and disease stress programs converge. Key references David Y, Castro IG, Schuldiner M. The Fast and the Furious: Golgi Contact Sites. Contact. 2021. DOI: 10.1177/25152564211034424. Maddison DC et al. COPI-regulated mitochondria-ER contact site formation maintains axonal integrity. Cell Reports. 2023. DOI: 10.1016/j.celrep.2023.112883. Diokmetzidou A, Scorrano L. Mitochondria–membranous organelle contacts at a glance. J Cell Sci. 2025. DOI: 10.1242/jcs.263895. Sarhadi TR, Panse JS, Nagotu S. Mind the gap: Methods to study membrane contact sites. Experimental Cell Research. 2023. DOI: 10.1016/j.yexcr.2023.113756

A new Focus article discusses the role that Foxp3 plays in establishing regulatory T cell identity and highlights the therapeutic potential of engineered #Treg cells for #autoimmune disorders. @R_Stadhouders @mieke65124955 scim.ag/4cHVthh

İki harfle onlarca kelimenin mantığını öğrenebilirsiniz.

Esta transformación de la basura es una auténtica locura

Cell-type-targeted mitochondrial transplantation rescues cell degeneration | Nature nature.com/articles/s4158…

Mitochondrial dysfunction underlies a wide spectrum of diseases—from neurodegeneration to heart failure. Yet, targeted delivery of healthy mitochondria has remained a major bottleneck. This Nature study introduces MitoCatch, a programmable system that enables cell-type-specific mitochondrial transplantation using engineered protein binders. � Nature Three modular strategies: MitoCatch-C: binders expressed on target cell surfaces MitoCatch-M: binders displayed on mitochondria MitoCatch-Bi: bispecific linkers bridging both � Nature Key outcomes: Efficient mitochondrial internalization Integration into cellular dynamics (fusion/fission) Functional rescue of degenerating cells This work defines a new paradigm: 👉 Precision organelle therapy 👉 Potential applications in heart failure, neurodegeneration, and aging biology 📚 Reference Cell-type-specific mitochondrial transplantation by programmable protein engineering Nature, 2026 DOI: 10.1038/s41586-026-10391-0

Mitochondrial fission promotes antibacterial defense via the mitochondrial unfolded protein response and inducible lipid droplets @SciImmunology science.org/doi/10.1126/sc… 🇦🇺

For decades, biology textbooks have enshrined a simple rule: DNA is made by copying a template. After one enzyme unzips a DNA double helix into separate strands, another called a polymerase builds a complementary sequence, base by base, for each strand. Presto: two copies of the original DNA. But new research into how bacteria defend themselves from viruses now shows this synthesis rule isn’t absolute. Now, a team describes a bacterial enzyme that synthesizes DNA without a nucleic acid template, using its own structure as a guide. Learn more: scim.ag/4tTc5IA @NewsfromScience

Krahn, Glick et al. @UChicago use budding yeast to examine membrane recycling at the Golgi apparatus. They describe an in vivo vesicle capture assay that reveals which resident Golgi proteins recycle together in the same vesicles. hubs.ly/Q04czhjb0

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