@article{22267,
  abstract     = {Thermal pollution, whether local or driven by global warming, threatens biodiversity in part through its detrimental effects on reproduction. Non-coding small RNAs (sRNAs) are crucial for maintaining germline developmental robustness under heat stress. Remarkably, we uncovered that neuronal sRNAs regulate germ cells’ thermotolerance, affecting both spermatogenic and oogenic germlines in a cell-non-autonomous manner. Furthermore, we demonstrate that, in RNAi mutants, an oxygen-sensing neural circuit, modulated by neuropeptide signaling, antagonizes germline maintenance, likely reflecting the nematode’s innate association of reduced oxygen levels with food availability and reproductive permissive environments. Finally, we provide evidence that laboratory-domesticated alleles of oxygen-response genes encoding neuropeptide receptor NPR-1 and hexacoordinated globin GLB-5 compromise germline thermotolerance. Hence, our findings raise the possibility that sensory perception, independent of direct environmental change, modulates germline integrity, highlighting a novel mechanism by which neural circuits integrate environmental information to safeguard reproductive fitness in fluctuating environments.},
  author       = {Ewe, Chee Kiang and Achache, Hanna and Schön, Hanna and Kontorovich, Leonid and Teichman, Guy and Weiss, Shir and Mogilevskaya, Anna and Valenski, Myriam and Anava, Sarit and Bardapurkar, Rutwik and Gingold, Hila and Posner, Rachel and Antonova, Olga and De Bono, Mario and Tzur, Yonatan B. and Rechavi, Oded},
  issn         = {1879-0445},
  journal      = {Current Biology},
  number       = {14},
  pages        = {3566--3579.e5},
  publisher    = {Elsevier},
  title        = {{Neuronal RNAi and oxygen-sensing circuit shape germline resilience to heat stress}},
  doi          = {10.1016/j.cub.2026.06.016},
  volume       = {36},
  year         = {2026},
}

@article{20929,
  abstract     = {Insulin/insulin-like growth factor signaling inhibits FOXO transcription factors to control development, homeostasis, and aging. Here, we use proximity labeling to identify proteins interacting with the C. elegans FOXO DAF-16. We show that in well-fed, unstressed animals harboring active insulin signaling, DAF-16 forms a complex with the PAR-1/MARK serine/threonine kinase, a key regulator of cell polarity. PAR-1 inhibits DAF-16 accumulation and promotes DAF-16 phosphorylation at S249, at a conserved motif that PAR-1/human MARK2 phosphorylates in vitro. DAF-2 insulin-like receptor signaling stimulates DAF-16 S249 phosphorylation, suggesting DAF-2 activates PAR-1. DAF-2 also promotes PAR-1 expression by inhibiting DAF-16. PAR-1 knockdown, or DAF-16 S249A, prolong lifespan, whereas phosphomimetic DAF-16 S249D suppresses the longevity of daf-2 mutants. At low insulin signaling, DAF-16 proximity labeling highlights transcription factors, chromatin regulators, and DNA repair proteins. One interactor, the zinc finger/homeobox protein ZFH-2/ZFHX3, forms a complex with DAF-16 and prolongs lifespan. Our work provides entry points for hypothesis-driven studies of FOXO function and longevity.},
  author       = {Artan, Murat and Schön, Hanna and De Bono, Mario},
  issn         = {2041-1723},
  journal      = {Nature Communications},
  publisher    = {Springer Nature},
  title        = {{Proximity labeling of DAF-16 FOXO highlights aging regulatory proteins}},
  doi          = {10.1038/s41467-025-66409-0},
  volume       = {16},
  year         = {2025},
}

@phdthesis{20167,
  author       = {Schön, Hanna},
  isbn         = {978-3-99078-061-9},
  issn         = {2663-337X},
  pages        = {171},
  publisher    = {Institute of Science and Technology Austria},
  title        = {{The ER complex SUTU-7/MACO-1 regulates the fate of mRNAs encoding GPCRs}},
  doi          = {10.15479/AT-ISTA-20167},
  year         = {2025},
}

@article{7957,
  abstract     = {Neurodevelopmental disorders (NDDs) are a class of disorders affecting brain development and function and are characterized by wide genetic and clinical variability. In this review, we discuss the multiple factors that influence the clinical presentation of NDDs, with particular attention to gene vulnerability, mutational load, and the two-hit model. Despite the complex architecture of
mutational events associated with NDDs, the various proteins involved appear to converge on common pathways, such as synaptic plasticity/function, chromatin remodelers and the mammalian target of rapamycin (mTOR) pathway. A thorough understanding of the mechanisms behind these pathways will hopefully lead to the identification of candidates that could be targeted for treatment approaches.},
  author       = {Parenti, Ilaria and Garcia Rabaneda, Luis E and Schön, Hanna and Novarino, Gaia},
  issn         = {1878-108X},
  journal      = {Trends in Neurosciences},
  number       = {8},
  pages        = {608--621},
  publisher    = {Elsevier},
  title        = {{Neurodevelopmental disorders: From genetics to functional pathways}},
  doi          = {10.1016/j.tins.2020.05.004},
  volume       = {43},
  year         = {2020},
}