Sara Orellana Munoz

• Munoz, Sara Orellana; Haberkorn, Chloé; Csoboz, Balint; Stelkens, Rike & Peris, David (2026). Mitochondrial inheritance as an important parameter for the rational design of synthetic yeast polyploids. BioRxiv. ISSN 0362-4331. doi: https:/www.biorxiv.org/content/10.64898/2026.09.22.753424v1. Fulltekst i vitenarkiv
• Balaguera, Nathalia Chica; Andersen, Aram Nikolai; Munoz, Sara Orellana; Llorente, Ignacio Garcia; P, Aurélie Nguéa & Nakken, Sigve [Vis alle 14 forfattere av denne artikkelen] (2026). Time-resolved functional genomics using deep learning reveals global hierarchical control of autophagy. Nature Cell Biology. ISSN 1465-7392. 28(3), s. 465–479. doi: 10.1038/s41556-025-01837-0. Fulltekst i vitenarkiv Vis sammendrag

  Recycling of cellular components through autophagy maintains homeostasis in changing nutrient environments. Although its core mechanisms are extensively studied, understanding of its systems-wide dynamic regulation remains limited, particularly regarding how autophagy is inactivated once nutrients are restored. Here we mapped the genetic network that controls activation and inactivation of autophagy during nitrogen changes by combining time-resolved high-content imaging, deep learning and latent feature analysis. This dataset, termed AutoDRY, categorizes 5,919 mutants based on nutrient response kinetics and their contributions to autophagosome formation and clearance. Integrating these profiles with functional and genetic network data uncovered hierarchical and multilayered control of autophagy and revealed multiple new regulatory pathways. Notably, we identified the retrograde pathway as a pivotal time-varying modulator that tunes the expression of core autophagy genes and plays a central role in autophagy inactivation. Together, this study establishes a systems-level resource to guide future investigations of autophagy.

• Klionsky, Daniel J.; Abdel-Aziz, Amal Kamal; Abdelfatah, Sara; Abdellatif, Mahmoud Khaled; Abdoli, Asghar & Abudu, Yakubu Princely [Vis alle 50 forfattere av denne artikkelen] (2021). Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition). Autophagy. ISSN 1554-8627. 17(1), s. 1–382. doi: https:/www.tandfonline.com/doi/full/10.1080/15548627.2020.1797280. Fulltekst i vitenarkiv
• Llorente, Ignacio Garcia; Munoz, Sara Orellana; Alonso, Lucia Ramos; Andersen, Aram Nikolai; Zimmermann, Christine & Eriksson, Jens [Vis alle 11 forfattere av denne artikkelen] (2021). Kel1 is a phosphorylation-regulated noise suppressor of the pheromone signaling pathway. Cell reports. 37(13), s. 1–20. doi: 10.1016/j.celrep.2021.110186. Fulltekst i vitenarkiv Vis sammendrag

  Mechanisms have evolved that allow cells to detect signals and generate an appropriate response. The accuracy of these responses relies on the ability of cells to discriminate between signal and noise. How cells filter noise in signaling pathways is not well understood. Here, we analyze noise suppression in the yeast pheromone signaling pathway and show that the poorly characterized protein Kel1 serves as a major noise suppressor and prevents cell death. At the molecular level, Kel1 prevents spontaneous activation of the pheromone response by inhibiting membrane recruitment of Ste5 and Far1. Only a hypophosphorylated form of Kel1 suppresses signaling, reduces noise, and prevents pheromone-associated cell death, and our data indicate that the MAPK Fus3 contributes to Kel1 phosphorylation. Taken together, Kel1 serves as a phospho-regulated suppressor of the pheromone pathway to reduce noise, inhibit spontaneous activation of the pathway, regulate mating efficiency, and prevent pheromone-associated cell death.

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• Munoz, Sara Orellana; Haberkorn, Chloé; Csoboz, Balint; Stelkens, Rike & Peris, David (2026). Mitochondrial–nuclear interactions shape hybrid physiology in Saccharomyces. Fulltekst i vitenarkiv
• Peris, David; Munoz, Sara Orellana; Csoboz, Balint; Sorribes-Daudén, Raquel; Vanacloig-Pedrós, Elena & Aguilar-Díaz, Alejandro [Vis alle 11 forfattere av denne artikkelen] (2025). FunGIALab: Connecting Fungal Diversity, Evolution, and Biotechnological Applications. Fulltekst i vitenarkiv

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