@article{MTMT:34779700,
	title = {Iterative oxidation by TET1 is required for reprogramming of imprinting control regions and patterning of mouse sperm hypomethylated regions},
	url = {https://m2.mtmt.hu/api/publication/34779700},
	author = {Prasasya, R.D. and Caldwell, B.A. and Liu, Z. and Wu, S. and Leu, N.A. and Fowler, J.M. and Cincotta, S.A. and Laird, D.J. and Kohli, R.M. and Bartolomei, M.S.},
	doi = {10.1016/j.devcel.2024.02.012},
	journal-iso = {DEV CELL},
	journal = {DEVELOPMENTAL CELL},
	unique-id = {34779700},
	issn = {1534-5807},
	abstract = {Ten-eleven translocation (TET) enzymes iteratively oxidize 5-methylcytosine (5mC) to generate 5-hydroxymethylcytosine (5hmC), 5-formylcytosine, and 5-carboxylcytosine to facilitate active genome demethylation. Whether these bases are required to promote replication-coupled dilution or activate base excision repair during mammalian germline reprogramming remains unresolved due to the inability to decouple TET activities. Here, we generated two mouse lines expressing catalytically inactive TET1 (Tet1-HxD) and TET1 that stalls oxidation at 5hmC (Tet1-V). Tet1 knockout and catalytic mutant primordial germ cells (PGCs) fail to erase methylation at select imprinting control regions and promoters of meiosis-associated genes, validating the requirement for the iterative oxidation of 5mC for complete germline reprogramming. TET1V and TET1HxD rescue most hypermethylation of Tet1−/− sperm, suggesting the role of TET1 beyond its oxidative capability. We additionally identify a broader class of hypermethylated regions in Tet1 mutant mouse sperm that depend on TET oxidation for reprogramming. Our study demonstrates the link between TET1-mediated germline reprogramming and sperm methylome patterning. © 2024 Elsevier Inc.},
	keywords = {DNA methylation; Imprinting; epigenetic; Reprogramming; Sperm methylome; tet enzyme; germline reprogramming; primordial germ cell establishment; sperm DNA methylation establishment},
	year = {2024},
	eissn = {1878-1551}
}

@article{MTMT:34773990,
	title = {Rim aperture of yeast autophagic membranes balances cargo inclusion with vesicle maturation},
	url = {https://m2.mtmt.hu/api/publication/34773990},
	author = {Shatz, O. and Fraiberg, M. and Isola, D. and Das, S. and Gogoi, O. and Polyansky, A. and Shimoni, E. and Dadosh, T. and Dezorella, N. and Wolf, S.G. and Elazar, Z.},
	doi = {10.1016/j.devcel.2024.02.002},
	journal-iso = {DEV CELL},
	journal = {DEVELOPMENTAL CELL},
	unique-id = {34773990},
	issn = {1534-5807},
	year = {2024},
	eissn = {1878-1551}
}

@article{MTMT:34814834,
	title = {Characterization of the human fetal gonad and reproductive tract by single-cell transcriptomics},
	url = {https://m2.mtmt.hu/api/publication/34814834},
	author = {Taelman, J. and Czukiewska, S.M. and Moustakas, I. and Chang, Y.W. and Hillenius, S. and van, der Helm T. and van, der Meeren L.E. and Mei, H. and Fan, X. and Chuva, de Sousa Lopes S.M.},
	doi = {10.1016/j.devcel.2024.01.006},
	journal-iso = {DEV CELL},
	journal = {DEVELOPMENTAL CELL},
	volume = {59},
	unique-id = {34814834},
	issn = {1534-5807},
	year = {2024},
	eissn = {1878-1551},
	pages = {529-544.e5}
}

@article{MTMT:34806990,
	title = {Aneuploidy-induced cellular behaviors: Insights from Drosophila},
	url = {https://m2.mtmt.hu/api/publication/34806990},
	author = {Joy, J. and Fusari, E. and Milán, M.},
	doi = {10.1016/j.devcel.2023.12.009},
	journal-iso = {DEV CELL},
	journal = {DEVELOPMENTAL CELL},
	volume = {59},
	unique-id = {34806990},
	issn = {1534-5807},
	year = {2024},
	eissn = {1878-1551},
	pages = {295-307}
}

@article{MTMT:34787241,
	title = {Dynamic palmitoylation of STX11 controls injury-induced fatty acid uptake to promote muscle regeneration},
	url = {https://m2.mtmt.hu/api/publication/34787241},
	author = {Wang, J. and Li, D.-L. and Zheng, L.-F. and Ren, S. and Huang, Z.-Q. and Tao, Y. and Liu, Z. and Shang, Y. and Pang, D. and Guo, H. and Zeng, T. and Wang, H.-R. and Huang, H. and Du, X. and Ye, H. and Zhou, H.-M. and Li, P. and Zhao, T.-J.},
	doi = {10.1016/j.devcel.2023.12.005},
	journal-iso = {DEV CELL},
	journal = {DEVELOPMENTAL CELL},
	volume = {59},
	unique-id = {34787241},
	issn = {1534-5807},
	abstract = {Different types of cells uptake fatty acids in response to different stimuli or physiological conditions; however, little is known about context-specific regulation of fatty acid uptake. Here, we show that muscle injury induces fatty acid uptake in muscle stem cells (MuSCs) to promote their proliferation and muscle regeneration. In humans and mice, fatty acids are mobilized after muscle injury. Through CD36, fatty acids function as both fuels and growth signals to promote MuSC proliferation. Mechanistically, injury triggers the translocation of CD36 in MuSCs, which relies on dynamic palmitoylation of STX11. Palmitoylation facilitates the formation of STX11/SNAP23/VAMP4 SANRE complex, which stimulates the fusion of CD36- and STX11-containing vesicles. Restricting fatty acid supply, blocking fatty acid uptake, or inhibiting STX11 palmitoylation attenuates muscle regeneration in mice. Our studies have identified a critical role of fatty acids in muscle regeneration and shed light on context-specific regulation of fatty acid sensing and uptake. © 2023 Elsevier Inc.},
	keywords = {Animals; Humans; metabolism; PALMITOYLATION; PALMITOYLATION; MICE; MUSCLE; ARTICLE; MOUSE; human; animal; controlled study; Cell Membrane; Cell Membrane; nonhuman; animal tissue; animal model; animal experiment; animal cell; Muscle, Skeletal; skeletal muscle; cell proliferation; regulatory mechanism; diet supplementation; Biological Transport; fatty acids; triacylglycerol; transport at the cellular level; fatty acid; fatty acid transport; mitogen activated protein kinase 3; mitogen activated protein kinase 1; Adipose Tissue; LIPIDOMICS; Muscles; myoblast; energy yield; octanoic acid; muscle regeneration; muscle regeneration; oxidative phosphorylation; muscle injury; Qa-SNARE Proteins; fatty acid oxidation; CD36 antigen; CD36 antigen; CD36; fat mass; transcription factor PAX7; lipoylation; lipoylation; Fatty acid uptake; 1,4 diamino 1,4 bis(2 aminophenylthio) 2,3 dicyanobutadiene; syntaxin; C2C12 cell line; Muscle growth; coimmunoprecipitation; CD36 Antigens; STX11; STX11 protein, human},
	year = {2024},
	eissn = {1878-1551},
	pages = {384-399.e5}
}

@article{MTMT:34614992,
	title = {Generation of heart and vascular system in rodents by blastocyst complementation},
	url = {https://m2.mtmt.hu/api/publication/34614992},
	author = {Coppiello, Giulia and Barlabe, Paula and Moya-Jodar, Marta and Abizanda, Gloria and Pogontke, Cristina and Barreda, Carolina and Iglesias, Elena and Linares, Javier and Arellano-Viera, Estibaliz and Larequi, Eduardo and Martin-Uriz, Patxi San and Carvajal-Vergara, Xonia and Pelacho, Beatriz and Mazo, Manuel Maria and Perez-Pomares, Jose Maria and Ruiz-Villalba, Adrian and Ullate-Agote, Asier and Prosper, Felipe and Aranguren, Xabier L.},
	doi = {10.1016/j.devcel.2023.10.008},
	journal-iso = {DEV CELL},
	journal = {DEVELOPMENTAL CELL},
	volume = {58},
	unique-id = {34614992},
	issn = {1534-5807},
	abstract = {Generating organs from stem cells through blastocyst complementation is a promising approach to meet the clinical need for transplants. In order to generate rejection-free organs, complementation of both parenchymal and vascular cells must be achieved, as endothelial cells play a key role in graft rejection. Here, we used a lineage-specific cell ablation system to produce mouse embryos unable to form both the cardiac and vascular systems. By mouse intraspecies blastocyst complementation, we rescued heart and vascular system development separately and in combination, obtaining complemented hearts with cardiomyocytes and endothelial cells of exogenous origin. Complemented chimeras were viable and reached adult stage, showing normal cardiac function and no signs of histopathological defects in the heart. Furthermore, we implemented the cell ablation system for rat-to-mouse blastocyst complementation, obtaining xenogeneic hearts whose cardiomyocytes were completely of rat origin. These results represent an advance in the experimentation towards the in vivo generation of transplantable organs.},
	year = {2024},
	eissn = {1878-1551},
	orcid-numbers = {Coppiello, Giulia/0000-0001-6896-1084; Moya-Jodar, Marta/0000-0003-4141-3509; Barreda, Carolina/0000-0003-2621-179X; Ullate-Agote, Asier/0000-0002-8595-7703}
}

@article{MTMT:34632223,
	title = {Spatiotemporal modulation of growth factors directs the generation of multilineage mouse embryonic stem cell-derived mammary organoids},
	url = {https://m2.mtmt.hu/api/publication/34632223},
	author = {Sahu, S. and Sahoo, S. and Sullivan, T. and O'Sullivan, T.N. and Turan, S. and Albaugh, M.E. and Burkett, S. and Tran, B. and Salomon, D.S. and Kozlov, S.V. and Koehler, K.R. and Jolly, M.K. and Sharan, S.K.},
	doi = {10.1016/j.devcel.2023.12.003},
	journal-iso = {DEV CELL},
	journal = {DEVELOPMENTAL CELL},
	volume = {59},
	unique-id = {34632223},
	issn = {1534-5807},
	abstract = {Ectodermal appendages, such as the mammary gland (MG), are thought to have evolved from hair-associated apocrine glands to serve the function of milk secretion. Through the directed differentiation of mouse embryonic stem cells (mESCs), here, we report the generation of multilineage ESC-derived mammary organoids (MEMOs). We adapted the skin organoid model, inducing the dermal mesenchyme to transform into mammary-specific mesenchyme via the sequential activation of Bone Morphogenetic Protein 4 (BMP4) and Parathyroid Hormone-related Protein (PTHrP) and inhibition of hedgehog (HH) signaling. Using single-cell RNA sequencing, we identified gene expression profiles that demonstrate the presence of mammary-specific epithelial cells, fibroblasts, and adipocytes. MEMOs undergo ductal morphogenesis in Matrigel and can reconstitute the MG in vivo. Further, we demonstrate that the loss of function in placode regulators LEF1 and TBX3 in mESCs results in impaired skin and MEMO generation. In summary, our MEMO model is a robust tool for studying the development of ectodermal appendages, and it provides a foundation for regenerative medicine and disease modeling. © 2023},
	keywords = {Animals; metabolism; MICE; MOUSE; animal; Cell Differentiation; Cell Differentiation; Epithelial Cells; Organoids; epithelium cell; Hedgehog Proteins; embryonic stem cell; mammary gland; Mammary Glands, Animal; sonic hedgehog protein; udder; Mouse embryonic stem cell; mouse embryonic stem cells; SINGLE-CELL TRANSCRIPTOMICS; Organoid; Organoid; ectodermal appendages},
	year = {2024},
	eissn = {1878-1551},
	pages = {175-186.e8}
}

@article{MTMT:34614804,
	title = {Sweat gland development requires an eccrine dermal niche and couples two epidermal programs},
	url = {https://m2.mtmt.hu/api/publication/34614804},
	author = {Dingwall, Heather L. and Tomizawa, Reiko R. and Aharoni, Adam and Hu, Peng and Qiu, Qi and Kokalari, Blerina and Martinez, Serenity M. and Donahue, Joan C. and Aldea, Daniel and Mendoza, Meryl and Glass, Ian A. and Wu, Hao and Kamberov, Yana G.},
	doi = {10.1016/j.devcel.2023.11.015},
	journal-iso = {DEV CELL},
	journal = {DEVELOPMENTAL CELL},
	volume = {59},
	unique-id = {34614804},
	issn = {1534-5807},
	abstract = {Eccrine sweat glands are indispensable for human thermoregulation and, similar to other mammalian skin appendages, form from multipotent epidermal progenitors. Limited understanding of how epidermal progenitors specialize to form these vital organs has precluded therapeutic efforts toward their regeneration. Herein, we applied single -nucleus transcriptomics to compare the expression content of wild -type, eccrine-forming mouse skin to that of mice harboring a skin -specific disruption of Engrailed 1 (En1), a transcription factor that promotes eccrine gland formation in humans and mice. We identify two concurrent but disproportionate epidermal transcriptomes in the early eccrine anlagen: one that is shared with hair follicles and one that is En1 dependent and eccrine specific. We demonstrate that eccrine development requires the induction of a dermal niche proximal to each developing gland in humans and mice. Our study defines the signatures of eccrine identity and uncovers the eccrine dermal niche, setting the stage for targeted regeneration and comprehensive skin repair.},
	year = {2024},
	eissn = {1878-1551},
	orcid-numbers = {Aldea, Daniel/0000-0001-5101-0194}
}

@article{MTMT:34588944,
	title = {Article Mechanical regulation of substrate adhesion and de-adhesion drives a cell-contractile wave during Drosophila tissue morphogenesis},
	url = {https://m2.mtmt.hu/api/publication/34588944},
	author = {Collinet, Claudio and Bailles, Anais and Dehapiot, Benoi and Lecuit, Thomas},
	doi = {10.1016/j.devcel.2023.11.022},
	journal-iso = {DEV CELL},
	journal = {DEVELOPMENTAL CELL},
	volume = {59},
	unique-id = {34588944},
	issn = {1534-5807},
	abstract = {During morphogenesis, mechanical forces induce large-scale deformations; yet, how forces emerge from cellular contractility and adhesion is unclear. In Drosophila embryos, a tissue-scale wave of actomyosin contractility coupled with adhesion to the surrounding vitelline membrane drives polarized tissue invagina-tion. We show that this process emerges subcellularly from the mechanical coupling between myosin II acti-vation and sequential adhesion/de-adhesion to the vitelline membrane. At the wavefront, integrin clusters an-chor the actin cortex to the vitelline membrane and promote activation of myosin II, which in turn enhances adhesion in a positive feedback. Following cell detachment, cortex contraction and advective flow amplify myosin II. Prolonged contact with the vitelline membrane prolongs the integrin-myosin II feedback, increases integrin adhesion, and thus slows down cell detachment and wave propagation. The angle of cell detachment depends on adhesion strength and sets the tensile forces required for detachment. Thus, we document how the interplay between subcellular mechanochemical feedback and geometry drives tissue morphogenesis.},
	year = {2024},
	eissn = {1878-1551},
	orcid-numbers = {Collinet, Claudio/0000-0002-8532-2601}
}

@article{MTMT:34430834,
	title = {An Arabidopsis Rab18 GTPase promotes autophagy by tethering ATG18a to the ER in response to nutrient starvation},
	url = {https://m2.mtmt.hu/api/publication/34430834},
	author = {Sun, Jiaqi and Shao, Yang and Wang, Songyang and Li, Xunzheng and Feng, Shuqing and Wang, Weina and Leroy, Pierre and Li, Chengyang and Zheng, Huanquan},
	doi = {10.1016/j.devcel.2023.11.006},
	journal-iso = {DEV CELL},
	journal = {DEVELOPMENTAL CELL},
	unique-id = {34430834},
	issn = {1534-5807},
	year = {2023},
	eissn = {1878-1551}
}