{"title":"What We Talk About When We Talk About Evolution","authors":"J. Torday","doi":"10.4137/CCI.S29840","DOIUrl":"https://doi.org/10.4137/CCI.S29840","url":null,"abstract":"Currently, the biologic sciences are a Tower of Babel, having become so highly specialized that one discipline cannot effectively communicate with another. A mechanism for evolution that integrates development and physiologic homeostasis phylogenetically has been identified—cell-cell interactions. By reducing this process to ligand-receptor interactions and their intermediate down-stream signaling partners, it is possible, for example, to envision the functional homologies between such seemingly disparate structures and functions as the lung alveolus and kidney glomerulus, the skin and brain, or the skin and lung. For example, by showing the continuum of the lung phenotype for gas exchange at the cell-molecular level, being selected for increased surface area by augmenting lung surfactant production and function in lowering surface tension, we have determined an unprecedented structural-functional continuum from proximate to ultimate causation in evolution. It is maintained that tracing the changes in structure and function that have occurred over both the short-term history of the organism (as ontogeny), and the long-term history of the organism (as phylogeny), and how the mechanisms shared in common can account for both biologic stability and novelty, will provide the key to understanding the mechanisms of evolution. We need to better understand evolution from its unicellular origins as the Big Bang of biology.","PeriodicalId":88848,"journal":{"name":"Cell communication insights","volume":"7 1","pages":"1 - 15"},"PeriodicalIF":0.0,"publicationDate":"2015-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70688850","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Identification of Signaling Protein Complexes by Parallel Affinity Precipitation Coupled with Mass Spectrometry.","authors":"Heng Lu, Qishan Lin, Jihe Zhao","doi":"10.4137/CCI.S12484","DOIUrl":"https://doi.org/10.4137/CCI.S12484","url":null,"abstract":"<p><p>Protein-protein interactions play a pivotal role in both inter- and intra-cellular signaling. Identification of signaling protein complexes can thus shed important new insights into cell communications. We developed a parallel affinity precipitation protocol to overcome the disadvantages of the tandem affinity purification procedure, such as the potential disruption of target protein conformation, subcellular localization or function by epitope tags, the potential need of large amounts of cell culture or generation of stable cell lines, and relatively long duration the two-step precipitation takes. This new simplified assay of protein interaction is quick, economic and specific. This paper describes the details in the design and method of the assay.</p>","PeriodicalId":88848,"journal":{"name":"Cell communication insights","volume":"5 ","pages":"1-7"},"PeriodicalIF":0.0,"publicationDate":"2013-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4137/CCI.S12484","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32351960","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The Evolution of Cell Communication: The Road not Taken.","authors":"J S Torday, V K Rehan","doi":"10.4137/cci.s2776","DOIUrl":"https://doi.org/10.4137/cci.s2776","url":null,"abstract":"<p><p>In the post-genomic era the complex problem of evolutionary biology can be tackled from the top-down, the bottom-up, or from the middle-out. Given the emergent and contingent nature of this process, we have chosen to take the latter approach, both as a mechanistic link to developmental biology and as a rational means of identifying signaling mechanisms based on their functional genomic significance. Using this approach, we have been able to configure a working model for lung evolution by reverse-engineering lung surfactant from the mammalian lung to the swim bladder of fish. Based on this archetypal cell-molecular model, we have reduced evolutionary biology to cell communication, starting with unicellular organisms communicating with the environment, followed by cell-cell communication to generate metazoa, culminating in the communication of genetic information between generations, i.e. reproduction. This model predicts the evolution of physiologic systems-including development, homeostasis, disease, regeneration/repair, and aging- as a logical consequence of biology reducing entropy. This approach provides a novel and robust way of formulating refutable, testable hypotheses to determine the ultimate origins and first principles of physiology, providing candidate genes for phenotypes hypothesized to have mediated evolutionary changes in structure and/or function. Ultimately, it will form the basis for predictive medicine and molecular bioethics, rather than merely showing associations between genes and pathology, which is an unequivocal Just So Story. In this new age of genomics, our reach must exceed our grasp.</p>","PeriodicalId":88848,"journal":{"name":"Cell communication insights","volume":"2 ","pages":"17-25"},"PeriodicalIF":0.0,"publicationDate":"2009-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4398024/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33235717","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Stephen P Higgins, Rohan Samarakoon, Craig E Higgins, Jennifer Freytag, Cynthia E Wilkins-Port, Paul J Higgins
{"title":"TGF-β1-Induced Expression of the Anti-Apoptotic PAI-1 Protein Requires EGFR Signaling.","authors":"Stephen P Higgins, Rohan Samarakoon, Craig E Higgins, Jennifer Freytag, Cynthia E Wilkins-Port, Paul J Higgins","doi":"10.4137/cci.s2775","DOIUrl":"10.4137/cci.s2775","url":null,"abstract":"<p><p>TGF-β1 and its target gene encoding plasminogen activator inhibitor-1 (PAI-1) are major regulators of capillary outgrowth, vessel maturation and angiogenic network stability. The increasing realization of the complexity of PAI-1 action in the vascular system requires analysis of specific signaling events that impact its expression in a physiologically-relevant cell system. PAI-1 was required for tubular differentiation and maintenance of cellular survival in complex gels since targeted disruption of PAI-1 synthesis or activity with antisense constructs or function-blocking antibodies resulted in network regression. Indeed, serum-deprivation-induced apoptosis of tubulogenic T2 cells was concentration-dependently inhibited by addition of a stable PAI-1 mutant protein consistent with the established pro-survival role of PAI-1 in vascular endothelial cells. PAI-1 induction and ERK pathway activation in response to TGF-β1 was attenuated by EGFR signaling blockade (with AG1478) or preincubation with the MMP/ADAM inhibitor GM6001. The combination of AG1478 + GM6001 completely ablated both responses suggesting that EGFR transactivation is important in PAI-1 gene control and may, at least partially, involve ligand shedding. TGF-β1-stimulated PAI-1 induction was preceded, in fact, by EGFR phosphorylation on Y845 (a src kinase target residue). EGFR1 knockdown with lentiviral shRNA constructs, moreover, effectively decreased (by >75%) TGF-β1-stimulated PAI-1 expression whereas infection with control (i.e. GFP) viruses had no effect. TGF-β1 failed to induce PAI-1 synthesis in EGFR-deficient fibroblasts while introduction of a wild-type EGFR1 construct in EGFR(-/-) cells rescued the PAI-1 response to TGF-β1 confirming, at a genetic level, the targeted knockdown data. The continued clarification of novel cooperative signaling cascades that impact expression of important angiogenic genes (e.g. PAI-1) may provide therapeutically useful targets to manage the pathophysiology of human neoplastic and vascular diseases.</p>","PeriodicalId":88848,"journal":{"name":"Cell communication insights","volume":"2 ","pages":"1-11"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2953848/pdf/nihms203162.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"29361448","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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