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Yeast Cell Signalling Pathways (Volume 2)
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Yeast Cell Signalling Pathways (Volume 2)

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

Deadline for manuscript submissions: closed (31 May 2023) | Viewed by 4623

Special Issue Editor

Dr. Vitor Teixeira

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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 Issues, Collections and Topics in MDPI journals

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 amplify it though coordinated activation of multiple protein complexes and signalling 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 just targets but also convey messages to other cells both near and far.

A new view of signalling networks as integrative systems is now emerging with the fast-evolving era of ‘omics’ that has been giving us a novel paradigm that by far surpasses the classical single-gene or protein-centric approach common in biological research, and carry us to a conceptual view of dynamically exchanging networks of chemical and protein interactions, where concepts of concentration, compartmentalization and phase transition, and diffusion are the foundation of interconnectivity and high throughput signalling responses, with compelling beauty and intricacy.

In this new special issue, we would like to highlight the dynamic nature of yeast signalling 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 submissions that pass pre-check are 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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21 pages, 1806 KiB  
Article
Iron Limitation Restores Autophagy and Increases Lifespan in the Yeast Model of Niemann–Pick Type C1
by Telma S. Martins, Rafaela S. Costa, Rita Vilaça, Carolina Lemos, Vitor Teixeira, Clara Pereira and Vítor Costa
Int. J. Mol. Sci. 2023, 24(7), 6221; https://doi.org/10.3390/ijms24076221 - 25 Mar 2023
Cited by 3 | Viewed by 2499
Abstract
Niemann–Pick type C1 (NPC1) is an endolysosomal transmembrane protein involved in the export of cholesterol and sphingolipids to other cellular compartments such as the endoplasmic reticulum and plasma membrane. NPC1 loss of function is the major cause of NPC disease, a rare lysosomal [...] Read more.
Niemann–Pick type C1 (NPC1) is an endolysosomal transmembrane protein involved in the export of cholesterol and sphingolipids to other cellular compartments such as the endoplasmic reticulum and plasma membrane. NPC1 loss of function is the major cause of NPC disease, a rare lysosomal storage disorder characterized by an abnormal accumulation of lipids in the late endosomal/lysosomal network, mitochondrial dysfunction, and impaired autophagy. NPC phenotypes are conserved in yeast lacking Ncr1, an orthologue of human NPC1, leading to premature aging. Herein, we performed a phosphoproteomic analysis to investigate the effect of Ncr1 loss on cellular functions mediated by the yeast lysosome-like vacuoles. Our results revealed changes in vacuolar membrane proteins that are associated mostly with vesicle biology (fusion, transport, organization), autophagy, and ion homeostasis, including iron, manganese, and calcium. Consistently, the cytoplasm to vacuole targeting (Cvt) pathway was increased in ncr1∆ cells and autophagy was compromised despite TORC1 inhibition. Moreover, ncr1∆ cells exhibited iron overload mediated by the low-iron sensing transcription factor Aft1. Iron deprivation restored the autophagic flux of ncr1∆ cells and increased its chronological lifespan and oxidative stress resistance. These results implicate iron overload on autophagy impairment, oxidative stress sensitivity, and cell death in the yeast model of NPC1. Full article
(This article belongs to the Special Issue Yeast Cell Signalling Pathways (Volume 2))
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12 pages, 2491 KiB  
Article
Inactivation of HAP4 Accelerates RTG-Dependent Osmoadaptation in Saccharomyces cerevisiae
by Maria Antonietta Di Noia, Pasquale Scarcia, Gennaro Agrimi, Ohiemi Benjamin Ocheja, Ehtisham Wahid, Isabella Pisano, Eleonora Paradies, Luigi Palmieri, Cataldo Guaragnella and Nicoletta Guaragnella
Int. J. Mol. Sci. 2023, 24(6), 5320; https://doi.org/10.3390/ijms24065320 - 10 Mar 2023
Cited by 3 | Viewed by 1818
Abstract
Mitochondrial RTG (an acronym for ReTroGrade) signaling plays a cytoprotective role under various intracellular or environmental stresses. We have previously shown its contribution to osmoadaptation and capacity to sustain mitochondrial respiration in yeast. Here, we studied the interplay between RTG2, the main [...] Read more.
Mitochondrial RTG (an acronym for ReTroGrade) signaling plays a cytoprotective role under various intracellular or environmental stresses. We have previously shown its contribution to osmoadaptation and capacity to sustain mitochondrial respiration in yeast. Here, we studied the interplay between RTG2, the main positive regulator of the RTG pathway, and HAP4, encoding the catalytic subunit of the Hap2-5 complex required for the expression of many mitochondrial proteins that function in the tricarboxylic acid (TCA) cycle and electron transport, upon osmotic stress. Cell growth features, mitochondrial respiratory competence, retrograde signaling activation, and TCA cycle gene expression were comparatively evaluated in wild type and mutant cells in the presence and in the absence of salt stress. We showed that the inactivation of HAP4 improved the kinetics of osmoadaptation by eliciting both the activation of retrograde signaling and the upregulation of three TCA cycle genes: citrate synthase 1 (CIT1), aconitase 1 (ACO1), and isocitrate dehydrogenase 1 (IDH1). Interestingly, their increased expression was mostly dependent on RTG2. Impaired respiratory competence in the HAP4 mutant does not affect its faster adaptive response to stress. These findings indicate that the involvement of the RTG pathway in osmostress is fostered in a cellular context of constitutively reduced respiratory capacity. Moreover, it is evident that the RTG pathway mediates peroxisomes–mitochondria communication by modulating the metabolic function of mitochondria in osmoadaptation. Full article
(This article belongs to the Special Issue Yeast Cell Signalling Pathways (Volume 2))
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