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Special Issue "Yeast Cell Signalling Pathways"

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Biochemistry".

Deadline for manuscript submissions: 30 September 2021.

Special Issue Editor

Prof. Dr. Vitor Teixeira
E-Mail Website
Guest Editor
Yeast Signalling Networks Group, i3s – Instituto de Investigação e Inovação em Saúde, Universidade do Port, Porto, Portugal
Interests: lipid and energy metabolism; lipid metabolic pathways; interorganelle membrane contact sites; organelle dysfunction in disease; aging; lipid-related diseases; molecular disease mechanisms in lipid disorders

Special Issue Information

Dear Colleagues,

In order to respond to metabolic and environmental cues, cells are equipped with a sophisticated array of receptors and proteins that are able to receive and transduce signals by triggering a chain of events that not only carries the input but also amplifies it though coordinated activation of multiple protein complexes and signaling effectors. The ability to integrate multiple signals into a unified action plan is, by far, one of the most open questions in the field. And, yet, cells aren’t simply targets but also convey messages to other cells both near and far.

A new view of signaling networks as integrative systems is now emerging with the fast-evolving era of ´omics´, that has served as a novel paradigm that has long surpassed the classical single-gene or protein-centric approach common in biological research, providing us with a conceptual view of dynamically exchanging networks of chemical and protein interactions, where concepts of concentration, compartmentalization, and phase transition and diffusion are at the foundation of interconnectivity and high-throughput signaling responses, with compelling beauty and intricacy.

In this Special Issue, we would like to highlight the dynamic nature of yeast signaling transduction with emphasis on (i) challenges on the extent of complexity that underlies biological responses and events, (ii) the specific and non-specific interactions of proteins with lipids and other proteins, (iii) expansive diversity of proteins and interaction/binding motifs and interfaces responsible for transducing signals, (iv) various therapeutic strategies arising from basic and applied research in signal transduction using this model system, and (v) emerging and novel areas in molecular medicine and rational drug design.

Dr. Vitor Teixeira
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • yeast
  • signal transduction
  • intracellular and intercellular communication
  • cell surface receptors
  • protein kinases and phosphatases
  • transcription factors
  • signal networks
  • posttranslational modification
  • biomedical research

Published Papers (2 papers)

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Research

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Article
Target of Rapamycin Complex 1 (TORC1), Protein Kinase A (PKA) and Cytosolic pH Regulate a Transcriptional Circuit for Lipid Droplet Formation
Int. J. Mol. Sci. 2021, 22(16), 9017; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22169017 - 20 Aug 2021
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Abstract
Lipid droplets (LDs) are ubiquitous organelles that fulfill essential roles in response to metabolic cues. The identification of several neutral lipid synthesizing and regulatory protein complexes have propelled significant advance on the mechanisms of LD biogenesis in the endoplasmic reticulum (ER). However, our [...] Read more.
Lipid droplets (LDs) are ubiquitous organelles that fulfill essential roles in response to metabolic cues. The identification of several neutral lipid synthesizing and regulatory protein complexes have propelled significant advance on the mechanisms of LD biogenesis in the endoplasmic reticulum (ER). However, our understanding of signaling networks, especially transcriptional mechanisms, regulating membrane biogenesis is very limited. Here, we show that the nutrient-sensing Target of Rapamycin Complex 1 (TORC1) regulates LD formation at a transcriptional level, by targeting DGA1 expression, in a Sit4-, Mks1-, and Sfp1-dependent manner. We show that cytosolic pH (pHc), co-regulated by the plasma membrane H+-ATPase Pma1 and the vacuolar ATPase (V-ATPase), acts as a second messenger, upstream of protein kinase A (PKA), to adjust the localization and activity of the major transcription factor repressor Opi1, which in turn controls the metabolic switch between phospholipid metabolism and lipid storage. Together, this work delineates hitherto unknown molecular mechanisms that couple nutrient availability and pHc to LD formation through a transcriptional circuit regulated by major signaling transduction pathways. Full article
(This article belongs to the Special Issue Yeast Cell Signalling Pathways)
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Review

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Review
Using Budding Yeast to Identify Molecules That Block Cancer Cell ‘Mitotic Slippage’ Only in the Presence of Mitotic Poisons
Int. J. Mol. Sci. 2021, 22(15), 7985; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22157985 - 26 Jul 2021
Viewed by 498
Abstract
Research on the budding yeast Saccharomyces cerevisiae has yielded fundamental discoveries on highly conserved biological pathways and yeast remains the best-studied eukaryotic cell in the world. Studies on the mitotic cell cycle and the discovery of cell cycle checkpoints in budding yeast has [...] Read more.
Research on the budding yeast Saccharomyces cerevisiae has yielded fundamental discoveries on highly conserved biological pathways and yeast remains the best-studied eukaryotic cell in the world. Studies on the mitotic cell cycle and the discovery of cell cycle checkpoints in budding yeast has led to a detailed, although incomplete, understanding of eukaryotic cell cycle progression. In multicellular eukaryotic organisms, uncontrolled aberrant cell division is the defining feature of cancer. Some of the most successful classes of anti-cancer chemotherapeutic agents are mitotic poisons. Mitotic poisons are thought to function by inducing a mitotic spindle checkpoint-dependent cell cycle arrest, via the assembly of the highly conserved mitotic checkpoint complex (MCC), leading to apoptosis. Even in the presence of mitotic poisons, some cancer cells continue cell division via ‘mitotic slippage’, which may correlate with a cancer becoming refractory to mitotic poison chemotherapeutic treatments. In this review, knowledge about budding yeast cell cycle control is explored to suggest novel potential drug targets, namely, specific regions in the highly conserved anaphase-promoting complex/cyclosome (APC/C) subunits Apc1 and/or Apc5, and in a specific N-terminal region in the APC/C co-factor cell division cycle 20 (Cdc20), which may yield molecules which block ‘mitotic slippage’ only in the presence of mitotic poisons. Full article
(This article belongs to the Special Issue Yeast Cell Signalling Pathways)
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