@article{19465,
  author       = {Bernecky, Carrie A},
  issn         = {1471-0080},
  journal      = {Nature Reviews Molecular Cell Biology},
  publisher    = {Springer Nature},
  title        = {{Understanding the machinery that reads the genome}},
  doi          = {10.1038/s41580-025-00844-1},
  volume       = {26},
  year         = {2025},
}

@article{19736,
  abstract     = {The phytohormone auxin is a major signal coordinating growth and development in plants. The variety of its effects arises from its ability to form local auxin maxima and gradients within tissues, generated through directional cell-to-cell transport and elaborate metabolic control. These auxin distribution patterns instruct cells in a context-dependent manner to undergo predefined developmental transitions. In this Review, we discuss advances in auxin action at the level of homeostasis and signalling. We highlight key insights into the structural basis of PIN-mediated intercellular auxin transport and explore two novel non-transcriptional auxin signalling mechanisms: one involving intracellular Ca2+ transients and another involving cell-surface auxin perception that mediates global, ultrafast phosphorylation. Furthermore, we examine emerging evidence indicating the involvement of cyclic adenosine monophosphate as a second messenger in the transcriptional auxin response. Together, these recent developments in auxin research have profoundly deepened our understanding of the complex and diverse activities of auxin in plant growth and development.},
  author       = {Vanneste, Steffen and Pei, Yuanrong and Friml, Jiří},
  issn         = {1471-0080},
  journal      = {Nature Reviews Molecular Cell Biology},
  publisher    = {Springer Nature},
  title        = {{Mechanisms of auxin action in plant growth and development}},
  doi          = {10.1038/s41580-025-00851-2},
  year         = {2025},
}

@article{10182,
  abstract     = {The mitochondrial oxidative phosphorylation system is central to cellular metabolism. It comprises five enzymatic complexes and two mobile electron carriers that work in a mitochondrial respiratory chain. By coupling the oxidation of reducing equivalents coming into mitochondria to the generation and subsequent dissipation of a proton gradient across the inner mitochondrial membrane, this electron transport chain drives the production of ATP, which is then used as a primary energy carrier in virtually all cellular processes. Minimal perturbations of the respiratory chain activity are linked to diseases; therefore, it is necessary to understand how these complexes are assembled and regulated and how they function. In this Review, we outline the latest assembly models for each individual complex, and we also highlight the recent discoveries indicating that the formation of larger assemblies, known as respiratory supercomplexes, originates from the association of the intermediates of individual complexes. We then discuss how recent cryo-electron microscopy structures have been key to answering open questions on the function of the electron transport chain in mitochondrial respiration and how supercomplexes and other factors, including metabolites, can regulate the activity of the single complexes. When relevant, we discuss how these mechanisms contribute to physiology and outline their deregulation in human diseases.},
  author       = {Vercellino, Irene and Sazanov, Leonid A},
  issn         = {1471-0080},
  journal      = {Nature Reviews Molecular Cell Biology},
  pages        = {141–161},
  publisher    = {Springer Nature},
  title        = {{The assembly, regulation and function of the mitochondrial respiratory chain}},
  doi          = {10.1038/s41580-021-00415-0},
  volume       = {23},
  year         = {2022},
}

@article{7009,
  abstract     = {Cell migration is essential for physiological processes as diverse as development, immune defence and wound healing. It is also a hallmark of cancer malignancy. Thousands of publications have elucidated detailed molecular and biophysical mechanisms of cultured cells migrating on flat, 2D substrates of glass and plastic. However, much less is known about how cells successfully navigate the complex 3D environments of living tissues. In these more complex, native environments, cells use multiple modes of migration, including mesenchymal, amoeboid, lobopodial and collective, and these are governed by the local extracellular microenvironment, specific modalities of Rho GTPase signalling and non- muscle myosin contractility. Migration through 3D environments is challenging because it requires the cell to squeeze through complex or dense extracellular structures. Doing so requires specific cellular adaptations to mechanical features of the extracellular matrix (ECM) or its remodelling. In addition, besides navigating through diverse ECM environments and overcoming extracellular barriers, cells often interact with neighbouring cells and tissues through physical and signalling interactions. Accordingly, cells need to call on an impressively wide diversity of mechanisms to meet these challenges. This Review examines how cells use both classical and novel mechanisms of locomotion as they traverse challenging 3D matrices and cellular environments. It focuses on principles rather than details of migratory mechanisms and draws comparisons between 1D, 2D and 3D migration.},
  author       = {Yamada, KM and Sixt, Michael K},
  issn         = {1471-0080},
  journal      = {Nature Reviews Molecular Cell Biology},
  number       = {12},
  pages        = {738–752},
  publisher    = {Springer Nature},
  title        = {{Mechanisms of 3D cell migration}},
  doi          = {10.1038/s41580-019-0172-9},
  volume       = {20},
  year         = {2019},
}