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Henderson B.,University College London | Fares M.A.,Trinity College Dublin | Fares M.A.,Institute Biologia Molecular Y Celular Of Plantas | Lund P.A.,University of Birmingham
Biological Reviews | Year: 2013

Chaperonin 60 is the prototypic molecular chaperone, an essential protein in eukaryotes and prokaryotes, whose sequence conservation provides an excellent basis for phylogenetic analysis. Escherichia coli chaperonin 60 (GroEL), the prototype of this family of proteins, has an established oligomeric-structure-based folding mechanism and a defined population of folding partners. However, there is a growing number of examples of chaperonin 60 proteins whose crystal structures and oligomeric composition are at variance with GroEL, suggesting that additional complexities in the protein-folding function of this protein should be expected. In addition, many organisms have multiple chaperonin 60 proteins, some of which have lost their protein-folding ability. It is emerging that this highly conserved protein has evolved a bewildering variety of additional biological functions - known as moonlighting functions - both within the cell and in the extracellular milieu. Indeed, in some organisms, it is these moonlighting functions that have been left after the loss of the protein-folding activity. This highlights the major paradox in the biology of chaperonin 60. This article reviews the relationship between the folding and non-folding (moonlighting) activities of the chaperonin 60 family and discusses current knowledge on their molecular evolution focusing on protein domains involved in the non-folding chaperonin functions in an attempt to understand the emerging biology of this evolutionarily ancient protein family.© 2013 Cambridge Philosophical Society. Source

de Visser J.A.G.M.,Wageningen University | Cooper T.F.,University of Houston | Elena S.F.,Institute Biologia Molecular Y Celular Of Plantas | Elena S.F.,Santa Fe Institute
Proceedings of the Royal Society B: Biological Sciences | Year: 2011

Since Bateson's discovery that genes can suppress the phenotypic effects of other genes, gene interactions-called epistasis-have been the topic of a vast research effort. Systems and developmental biologists study epistasis to understand the genotype-phenotype map, whereas evolutionary biologists recognize the fundamental importance of epistasis for evolution. Depending on its form, epistasis may lead to divergence and speciation, provide evolutionary benefits to sex and affect the robustness and evolvability of organisms. That epistasis can itself be shaped by evolution has only recently been realized. Here, we review the empirical pattern of epistasis, and some of the factors that may affect the form and extent of epistasis. Based on their divergent consequences, we distinguish between interactions with or without mean effect, and those affecting the magnitude of fitness effects or their sign. Empirical work has begun to quantify epistasis in multiple dimensions in the context of metabolic and fitness landscape models.We discuss possible proximate causes (such as protein function and metabolic networks) and ultimate factors (including mutation, recombination, and the importance of natural selection and genetic drift). We conclude that, in general, pleiotropy is an important prerequisite for epistasis, and that epistasis may evolve as an adaptive or intrinsic consequence of changes in genetic robustness and evolvability. © 2011 The Royal Society. Source

Mushegian A.R.,National Science Foundation | Elena S.F.,Institute Biologia Molecular Y Celular Of Plantas | Elena S.F.,Santa Fe Institute
Virology | Year: 2015

Homologs of Tobacco mosaic virus 30K cell-to-cell movement protein are encoded by diverse plant viruses. Mechanisms of action and evolutionary origins of these proteins remain obscure. We expand the picture of conservation and evolution of the 30K proteins, producing sequence alignment of the 30K superfamily with the broadest phylogenetic coverage thus far and illuminating structural features of the core all-beta fold of these proteins. Integrated copies of pararetrovirus 30K movement genes are prevalent in euphyllophytes, with at least one copy intact in nearly every examined species, and mRNAs detected for most of them. Sequence analysis suggests repeated integrations, pseudogenizations, and positive selection in those provirus genes. An unannotated 30K-superfamily gene in Arabidopsis thaliana genome is likely expressed as a fusion with the At1g37113 transcript. This molecular background of endopararetrovirus gene products in plants may change our view of virus infection and pathogenesis, and perhaps of cellular homeostasis in the hosts. © 2014. Source

Cutler S.R.,University of California at Riverside | Rodriguez P.L.,Institute Biologia Molecular Y Celular Of Plantas | Finkelstein R.R.,University of California at Santa Barbara | Abrams S.R.,National Research Council Canada
Annual Review of Plant Biology | Year: 2010

Abscisic acid (ABA) regulates numerous developmental processes and adaptive stress responses in plants. Many ABA signaling components have been identified, but their interconnections and a consensus on the structure of the ABA signaling network have eluded researchers. Recently, several advances have led to the identification of ABA receptors and their three-dimensional structures, and an understanding of how key regulatory phosphatase and kinase activities are controlled by ABA. A new model for ABA action has been proposed and validated, in which the soluble PYR/PYL/RCAR receptors function at the apex of a negative regulatory pathway to directly regulate PP2C phosphatases, which in turn directly regulate SnRK2 kinases. This model unifies many previously defined signaling components and highlights the importance of future work focused on defining the direct targets of SnRK2s and PP2Cs, dissecting the mechanisms of hormone interactions (i.e., cross talk) and defining connections between this new negative regulatory pathway and other factors implicated in ABA signaling. Copyright © 2010 by Annual Reviews. All rights reserved. Source

Lalic J.,Institute Biologia Molecular Y Celular Of Plantas | Elena S.F.,Institute Biologia Molecular Y Celular Of Plantas | Elena S.F.,Santa Fe Institute
Biology Letters | Year: 2013

How, and to what extent, does the environment influence the way mutations interact? Do environmental changes affect both the sign and the magnitude of epistasis? Are there any correlations between environments in the variability, sign or magnitude of epistasis? Very few studies have tackled these questions. Here, we addressed them in the context of viral emergence. Most emerging viruses are RNA viruses with small genomes, overlapping reading frames and multifunctional proteins for which epistasis is abundant. Understanding the effect of host species in the sign and magnitude of epistasis will provide insights into the evolutionary ecology of infectious diseases and the predictability of viral emergence. © 2012 The Author(s) Published by the Royal Society. All rights reserved. Source

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