13
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Transcriptomic analysis of regulatory pathways involved in female reproductive physiology of Rhodnius prolixus under different nutritional states

      research-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          The triatomine Rhodnius prolixus, a vector of the etiological agent of Chagas disease, has long been used as model to understand important aspects of insect physiology. Despite this history, the impact of the nutritional state on regulatory pathways associated with reproductive performance in triatomines has never been studied. The insulin-like peptide/target of rapamycin (ILP/ToR) signaling pathway is typically responsible for detecting and interpreting nutrient levels. Here, we analyzed transcriptomes from the central nervous system, fat bodies and ovaries of adult females in unfed and fed conditions, with a focus on the ILP/ToR signaling. The results show an up-regulation of transcripts involved in ILP/ToR signaling in unfed insects. However, we demonstrate that this signaling is only activated in tissues from fed insects. Moreover, we report that FoxO (forkhead box O) factor, which regulates longevity via ILP signaling, is responsible for the up-regulation of transcripts related with ILP/ToR signaling in unfed insects. As a consequence, we reveal that unfed females are in a sensitized state to respond to an increase of ILP levels by rapidly activating ILP/ToR signaling. This is the first analysis that correlates gene expression and protein activation of molecules involved with ILP/ToR signaling in R. prolixus females in different nutritional states.

          Related collections

          Most cited references45

          • Record: found
          • Abstract: found
          • Article: not found

          Role and regulation of starvation-induced autophagy in the Drosophila fat body.

          In response to starvation, eukaryotic cells recover nutrients through autophagy, a lysosomal-mediated process of cytoplasmic degradation. Autophagy is known to be inhibited by TOR signaling, but the mechanisms of autophagy regulation and its role in TOR-mediated cell growth are unclear. Here, we show that signaling through TOR and its upstream regulators PI3K and Rheb is necessary and sufficient to suppress starvation-induced autophagy in the Drosophila fat body. In contrast, TOR's downstream effector S6K promotes rather than suppresses autophagy, suggesting S6K downregulation may limit autophagy during extended starvation. Despite the catabolic potential of autophagy, disruption of conserved components of the autophagic machinery, including ATG1 and ATG5, does not restore growth to TOR mutant cells. Instead, inhibition of autophagy enhances TOR mutant phenotypes, including reduced cell size, growth rate, and survival. Thus, in cells lacking TOR, autophagy plays a protective role that is dominant over its potential role as a growth suppressor.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            The PTEN-PI3K pathway: of feedbacks and cross-talks.

            The tumor suppressor PTEN was originally identified as a negative regulator of the phosphoinositide 3-kinase (PI3K) signaling, a main regulator of cell growth, metabolism and survival. Yet this function of PTEN is extremely relevant for its tumor-suppressive ability, albeit the recent characterization of many PI3K-independent tumor-suppressive activities. PI3K-mediated PIP(3) production leads to the activation of the canonical AKT-mTORC1 pathway. The implications of this signaling cascade in health and disease have been underscored by the high number of regulators within the pathway whose alterations give rise to different malignancies, including familiar syndromes, metabolic dysfunctions and cancer. Moreover, PI3K is tightly buffered at multiple levels by downstream components, which have turned this signaling pathway literally upside down. PI3K and its downstream components in turn cross-talk with a number of other pathways, thereby leading to a complex network of signals that may have dramatic consequences when perturbed. Here, we review the current status of the PTEN-PI3K signaling pathway with special emphasis on the most recent data on targets and regulation of the PTEN-PI3K axis. This provides novel provocative therapeutic implications based on the targeted modulation of PI3K-cross-talking signals.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Biochemical and cellular properties of insulin receptor signalling.

              The mechanism of insulin action is a central theme in biology and medicine. In addition to the rather rare condition of insulin deficiency caused by autoimmune destruction of pancreatic β-cells, genetic and acquired abnormalities of insulin action underlie the far more common conditions of type 2 diabetes, obesity and insulin resistance. The latter predisposes to diseases ranging from hypertension to Alzheimer disease and cancer. Hence, understanding the biochemical and cellular properties of insulin receptor signalling is arguably a priority in biomedical research. In the past decade, major progress has led to the delineation of mechanisms of glucose transport, lipid synthesis, storage and mobilization. In addition to direct effects of insulin on signalling kinases and metabolic enzymes, the discovery of mechanisms of insulin-regulated gene transcription has led to a reassessment of the general principles of insulin action. These advances will accelerate the discovery of new treatment modalities for diabetes.
                Bookmark

                Author and article information

                Contributors
                jimenal.leyria@utoronto.ca
                Journal
                Sci Rep
                Sci Rep
                Scientific Reports
                Nature Publishing Group UK (London )
                2045-2322
                10 July 2020
                10 July 2020
                2020
                : 10
                : 11431
                Affiliations
                ISNI 0000 0001 2157 2938, GRID grid.17063.33, Department of Biology, , University of Toronto Mississauga, ; Mississauga, ON Canada
                Article
                67932
                10.1038/s41598-020-67932-4
                7351778
                32651410
                9de8e86a-eb63-421b-bacb-a6b6da5b2dc7
                © The Author(s) 2020

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

                History
                : 10 February 2020
                : 16 June 2020
                Funding
                Funded by: This research was supported through NSERC Discovery grants to A.B.L. and I.O.
                Categories
                Article
                Custom metadata
                © The Author(s) 2020

                Uncategorized
                reproductive biology,transcriptomics,molecular biology,physiology
                Uncategorized
                reproductive biology, transcriptomics, molecular biology, physiology

                Comments

                Comment on this article