Insights into the individual evolutionary origins of Yersinia virulence factor effector proteins

Plasmid ◽  
2021 ◽  
Vol 114 ◽  
pp. 102562
Author(s):  
Veronica R. Moorman ◽  
James I. Cohen
2011 ◽  
Vol 77 (13) ◽  
pp. 4669-4675 ◽  
Author(s):  
Dawn C. Bisi ◽  
David J. Lampe

ABSTRACTThe insect-vectored disease malaria is a major world health problem. New control strategies are needed to supplement the current use of insecticides and medications. A genetic approach can be used to inhibit development of malaria parasites (Plasmodiumspp.) in the mosquito host. We hypothesized thatPantoea agglomerans, a bacterial symbiont ofAnophelesmosquitoes, could be engineered to express and secrete anti-Plasmodiumeffector proteins, a strategy termed paratransgenesis. To this end, plasmids that include thepelBorhlyAsecretion signals from the genes of related species (pectate lyase fromErwinia carotovoraand hemolysin A fromEscherichia coli, respectively) were created and tested for their efficacy in secreting known anti-Plasmodiumeffector proteins (SM1, anti-Pbs21, and PLA2) inP. agglomeransandE. coli.P. agglomeranssuccessfully secreted HlyA fusions of anti-Pbs21 and PLA2, and these strains are under evaluation for anti-Plasmodiumactivity in infected mosquitoes. Varied expression and/or secretion of the effector proteins was observed, suggesting that the individual characteristics of a particular effector may require empirical testing of several secretion signals. Importantly, those strains that secreted efficiently grew as well as wild-type strains under laboratory conditions and, thus, may be expected to be competitive with the native microbiota in the environment of the mosquito midgut.


2021 ◽  
pp. jeb.238493
Author(s):  
Caroline H. Brighton ◽  
Katherine E. Chapman ◽  
Nicholas C. Fox ◽  
Graham K. Taylor

The aerial hunting behaviours of birds are strongly influenced by flight morphology and ecology, but little is known of how this relates to the behavioural algorithms guiding flight. Here we use GPS loggers to record the attack trajectories of captive-bred Gyrfalcons (Falco rusticolus) during their maiden flights against robotic aerial targets, which we compare to existing flight data from Peregrines (Falco peregrinus). The attack trajectories of both species are well modelled by a proportional navigation (PN) guidance law, which commands turning in proportion to the angular rate of the line-of-sight to target, at a guidance gain. However, naïve Gyrfalcons operate at significantly lower values of N than Peregrines, producing slower turning and a longer path to intercept. Gyrfalcons are less manoeuvrable than Peregrines, but physical constraint is insufficient to explain the lower values of N we found, which may reflect either the inexperience of the individual birds or ecological adaptation at the species level. For example, low values of N promote the tail-chasing behaviour that is typical of wild Gyrfalcons and which apparently serves to tire their prey in a prolonged high-speed pursuit. Likewise, during close pursuit of typical fast evasive prey, PN will be less prone to being thrown off by erratic target manoeuvres at low guidance gain. The fact that low-gain PN successfully models the maiden attack flights of Gyrfalcons suggests that this behavioural algorithm is embedded in a guidance pathway ancestral to the clade containing Gyrfalcons and Peregrines, though perhaps with much deeper evolutionary origins.


2020 ◽  
Vol 8 (4) ◽  
pp. 576
Author(s):  
Nicole A. Lerminiaux ◽  
Keith D. MacKenzie ◽  
Andrew D. S. Cameron

Salmonella Pathogenicity Island 1 (SPI-1) encodes a type three secretion system (T3SS), effector proteins, and associated transcription factors that together enable invasion of epithelial cells in animal intestines. The horizontal acquisition of SPI-1 by the common ancestor of all Salmonella is considered a prime example of how gene islands potentiate the emergence of new pathogens with expanded niche ranges. However, the evolutionary history of SPI-1 has attracted little attention. Here, we apply phylogenetic comparisons across the family Enterobacteriaceae to examine the history of SPI-1, improving the resolution of its boundaries and unique architecture by identifying its composite gene modules. SPI-1 is located between the core genes fhlA and mutS, a hotspot for the gain and loss of horizontally acquired genes. Despite the plasticity of this locus, SPI-1 demonstrates stable residency of many tens of millions of years in a host genome, unlike short-lived homologous T3SS and effector islands including Escherichia ETT2, Yersinia YSA, Pantoea PSI-2, Sodalis SSR2, and Chromobacterium CPI-1. SPI-1 employs a unique series of regulatory switches, starting with the dedicated transcription factors HilC and HilD, and flowing through the central SPI-1 regulator HilA. HilA is shared with other T3SS, but HilC and HilD may have their evolutionary origins in Salmonella. The hilA, hilC, and hilD gene promoters are the most AT-rich DNA in SPI-1, placing them under tight control by the transcriptional repressor H-NS. In all Salmonella lineages, these three promoters resist amelioration towards the genomic average, ensuring strong repression by H-NS. Hence, early development of a robust and well-integrated regulatory network may explain the evolutionary stability of SPI-1 compared to T3SS gene islands in other species.


Kybernetes ◽  
2016 ◽  
Vol 45 (8) ◽  
pp. 1292-1307 ◽  
Author(s):  
Jorge Navarro ◽  
Raquel del Moral ◽  
Pedro C. Marijuán

Purpose The purpose of this paper is to present a new core hypothesis on laughter. It has been built by putting together ideas from several disciplines: neurodynamics, evolutionary neurobiology, social networks, and communication studies. The hypothesis focusses on the social nature of laughter and contributes to ascertain its evolutionary origins in connection with the cognitive and social-emotional functions it performs. Design/methodology/approach An in-depth examination of laughter in the social communication context and along the life cycle of the individual is performed. This instinctive behaviour that appears as a “virtual”, non-physical form of “grooming” would serve as a bond-making instrument in human groups. Further, the neurodynamic events underlying laughter production – and particularly the form of the neural entropy gradients – are congruent with a sentic hypothesis about the different emotional contents of laughter and their specific effects on bonding dynamics. Findings The new behavioural and neurodynamic tenets introduced about this unusual sound feature of our species justify the ubiquitous presence it has in social interactions at large and along the life cycle of the individual. Laughter, far from being a curious evolutionary relic or a rather inconsequential innate behaviour, should be considered as a highly efficient tool for inter-individual problem solving and for maintenance of social bonds. Originality/value Laughter, the authors would conclude, has been evolutionarily kept and augmented as an optimized tool for unconscious cognitive-emotional problem solving, and at the same time as a useful way to preserve the essential fabric of social bonds in close-knit groups and within human societies at large.


2016 ◽  
Vol 113 (21) ◽  
pp. 5976-5981 ◽  
Author(s):  
Sabrina Engesser ◽  
Amanda R. Ridley ◽  
Simon W. Townsend

Language’s expressive power is largely attributable to its compositionality: meaningful words are combined into larger/higher-order structures with derived meaning. Despite its importance, little is known regarding the evolutionary origins and emergence of this syntactic ability. Although previous research has shown a rudimentary capability to combine meaningful calls in primates, because of a scarcity of comparative data, it is unclear to what extent analog forms might also exist outside of primates. Here, we address this ambiguity and provide evidence for rudimentary compositionality in the discrete vocal system of a social passerine, the pied babbler (Turdoides bicolor). Natural observations and predator presentations revealed that babblers produce acoustically distinct alert calls in response to close, low-urgency threats and recruitment calls when recruiting group members during locomotion. On encountering terrestrial predators, both vocalizations are combined into a “mobbing sequence,” potentially to recruit group members in a dangerous situation. To investigate whether babblers process the sequence in a compositional way, we conducted systematic experiments, playing back the individual calls in isolation as well as naturally occurring and artificial sequences. Babblers reacted most strongly to mobbing sequence playbacks, showing a greater attentiveness and a quicker approach to the loudspeaker, compared with individual calls or control sequences. We conclude that the sequence constitutes a compositional structure, communicating information on both the context and the requested action. Our work supports previous research suggesting combinatoriality as a viable mechanism to increase communicative output and indicates that the ability to combine and process meaningful vocal structures, a basic syntax, may be more widespread than previously thought.


2006 ◽  
Vol 34 (4) ◽  
pp. 504-509 ◽  
Author(s):  
E. Huston ◽  
T.M. Houslay ◽  
G.S. Baillie ◽  
M.D. Houslay

Specificity of cAMP signalling pathways has shown that the intracellular targeting of the individual components confers a three-dimensional context to the signalling paradigms in which they can exquisitely control the specificity of the outcome of the signal. Pivotal to this paradigm is degradation of cAMP by sequestered PDEs (phosphodiesterases). cAMP rapidly diffuses within cells and, without the action of spatially confined PDE populations, cAMP gradients could not be formed and shaped within cells so as to regulate targeted effector proteins. Of particular importance in regulating compartmentalized cAMP signalling are isoforms of the PDE4 family, which are individually defined by unique N-terminal regions. We have developed and pioneered the concept that a major function of this N-terminal region is to confer intracellular targeting of particular PDE4 isoforms on specific signalling complexes and intracellular locations. The paradigm for this concept developed from our original studies on the PDE4A1 (RD1) isoform. The N-terminal region unique to PDE4A1 consists of two well-defined helical regions separated by a mobile hinge region. Helix-2 provides the core membrane-insertion module, with helix-1 facilitating membrane association and fidelity of targeting in living cells. The irreversible, Ca2+-dependent insertion of the N-terminal region of PDE4A1 into membranes provides ‘long-term’ memory of cell activation.


2018 ◽  
Author(s):  
Eriko Matsuo ◽  
Yuji Inagaki

Background: The ancestral dinoflagellate most likely established a peridinin-containing plastid, which has been inherited to the extant photosynthetic descendants. However, kareniacean dinoflagellates and Lepidodinium species were known to bear “non-canonical” plastids lacking peridinin, which were established through a haptophyte and a green algal endosymbioses, respectively. For plastid function and maintenance, the aforementioned dinoflagellates were known to use nucleus-encoded proteins vertically inherited from the ancestral dinoflagellates (vertically inherited- or VI-type), and those acquired from non-dinoflagellate organisms including the endosymbionts. These observations indicated that the proteomes of the non-canonical plastids derived from a haptophyte and a green alga were modified by “exogenous” genes acquired from non-dinoflagellate organisms. However, there was no systematic evaluation addressing how “exogenous” genes reshaped individual metabolic pathways localized in a non-canonical plastid. Results: In this study, we surveyed transcriptomic data from two kareniacean species [Karenia (Ke.) brevis and Karlodinium (Kl.) veneficum] and Lepidodinium chlorophorum, and identified proteins involved in three plastid metabolic pathways synthesizing chlorophyll a (Chl a), heme and isopentenyl diphosphate (IPP). The origins of the individual proteins of our interest were investigated, and assessed how the three pathways were modified before and after the algal endosymbioses, which gave rise to the current non-canonical plastids. We observed a clear difference in the contribution of VI-type proteins across the three pathways. In both Ke. brevis/Kl. veneficum and L. chlorophorum, we observed a substantial contribution of VI-type proteins to the IPP and heme biosyntheses. In sharp contrast, VI-type protein was barely detected in the Chl a biosynthesis in the three dinoflagellates. Discussion: Pioneering works hypothesized that the ancestral kareniacean species had lost the photosynthetic activity prior to haptophyte endosymbiosis. The absence of VI-type proteins in the Chl a biosynthetic pathway in Ke. brevis or Kl. veneficum is in good agreement with the putative non-photosynthetic nature proposed for their ancestor. The dominance of proteins with haptophyte origin in the Ke. brevis/Kl. veneficum pathway suggests that their ancestor rebuilt the particular pathway by genes acquired from the endosymbiont. Likewise, we here propose that the ancestral Lepidodinium likely experienced a non-photosynthetic period and discarded the Chl a biosynthetic pathway mostly prior to the green algal endosymbiosis. In the subsequent evolution, L. chlorophorum rebuilt the pathway by genes transferred from phylogenetically diverse organisms, rather than the green algal endosymbiont. We explore the reasons why green algal genes were barely utilized to reconstruct the L. chlorophorum pathway.


2018 ◽  
Author(s):  
Eriko Matsuo ◽  
Yuji Inagaki

Background: The ancestral dinoflagellate most likely established a peridinin-containing plastid, which has been inherited to the extant photosynthetic descendants. However, kareniacean dinoflagellates and Lepidodinium species were known to bear “non-canonical” plastids lacking peridinin, which were established through a haptophyte and a green algal endosymbioses, respectively. For plastid function and maintenance, the aforementioned dinoflagellates were known to use nucleus-encoded proteins vertically inherited from the ancestral dinoflagellates (vertically inherited- or VI-type), and those acquired from non-dinoflagellate organisms including the endosymbionts. These observations indicated that the proteomes of the non-canonical plastids derived from a haptophyte and a green alga were modified by “exogenous” genes acquired from non-dinoflagellate organisms. However, there was no systematic evaluation addressing how “exogenous” genes reshaped individual metabolic pathways localized in a non-canonical plastid. Results: In this study, we surveyed transcriptomic data from two kareniacean species [Karenia (Ke.) brevis and Karlodinium (Kl.) veneficum] and Lepidodinium chlorophorum, and identified proteins involved in three plastid metabolic pathways synthesizing chlorophyll a (Chl a), heme and isopentenyl diphosphate (IPP). The origins of the individual proteins of our interest were investigated, and assessed how the three pathways were modified before and after the algal endosymbioses, which gave rise to the current non-canonical plastids. We observed a clear difference in the contribution of VI-type proteins across the three pathways. In both Ke. brevis/Kl. veneficum and L. chlorophorum, we observed a substantial contribution of VI-type proteins to the IPP and heme biosyntheses. In sharp contrast, VI-type protein was barely detected in the Chl a biosynthesis in the three dinoflagellates. Discussion: Pioneering works hypothesized that the ancestral kareniacean species had lost the photosynthetic activity prior to haptophyte endosymbiosis. The absence of VI-type proteins in the Chl a biosynthetic pathway in Ke. brevis or Kl. veneficum is in good agreement with the putative non-photosynthetic nature proposed for their ancestor. The dominance of proteins with haptophyte origin in the Ke. brevis/Kl. veneficum pathway suggests that their ancestor rebuilt the particular pathway by genes acquired from the endosymbiont. Likewise, we here propose that the ancestral Lepidodinium likely experienced a non-photosynthetic period and discarded the Chl a biosynthetic pathway mostly prior to the green algal endosymbiosis. In the subsequent evolution, L. chlorophorum rebuilt the pathway by genes transferred from phylogenetically diverse organisms, rather than the green algal endosymbiont. We explore the reasons why green algal genes were barely utilized to reconstruct the L. chlorophorum pathway.


2016 ◽  
Vol 283 (1822) ◽  
pp. 20152128 ◽  
Author(s):  
Sarah Barfield ◽  
Galina V. Aglyamova ◽  
Mikhail V. Matz

The ability to segregate a committed germ stem cell (GSC) lineage distinct from somatic cell lineages is a characteristic of bilaterian Metazoans. However, the occurrence of GSC lineage specification in basally branching Metazoan phyla, such as Cnidaria, is uncertain. Without an independently segregated GSC lineage, germ cells and their precursors must be specified throughout adulthood from continuously dividing somatic stem cells, generating the risk of propagating somatic mutations within the individual and its gametes. To address the potential for existence of a GSC lineage in Anthozoa, the sister-group to all remaining Cnidaria, we identified moderate- to high-frequency somatic mutations and their potential for gametic transfer in the long-lived coral Orbicella faveolata (Anthozoa, Cnidaria) using a 2b-RAD sequencing approach. Our results demonstrate that somatic mutations can drift to high frequencies (up to 50%) and can also generate substantial intracolonial genetic diversity. However, these somatic mutations are not transferable to gametes, signifying the potential for an independently segregated GSC lineage in O. faveolata. In conjunction with previous research on germ cell development in other basally branching Metazoan species, our results suggest that the GSC system may be a Eumetazoan characteristic that evolved in association with the emergence of greater complexity in animal body plan organization and greater specificity of stem cell functions.


2020 ◽  
Vol 375 (1796) ◽  
pp. 20190325 ◽  
Author(s):  
Ricard Solé ◽  
Sergi Valverde

A common trait of complex systems is that they can be represented by means of a network of interacting parts. It is, in fact, the network organization (more than the parts) that largely conditions most higher-level properties, which are not reducible to the properties of the individual parts. Can the topological organization of these webs provide some insight into their evolutionary origins? Both biological and artificial networks share some common architectural traits. They are often heterogeneous and sparse, and most exhibit different types of correlations, such as nestedness, modularity or hierarchical patterns. These properties have often been attributed to the selection of functionally meaningful traits. However, a proper formulation of generative network models suggests a rather different picture. Against the standard selection–optimization argument, some networks reveal the inevitable generation of complex patterns resulting from reuse and can be modelled using duplication–rewiring rules lacking functionality. These give rise to the observed heterogeneous, scale-free and modular architectures. Here, we examine the evidence for tinkering in cellular, technological and ecological webs and its impact in shaping their architecture. Our analysis suggests a serious consideration of the role played by selection as the origin of network topology. Instead, we suggest that the amplification processes associated with reuse might shape these graphs at the topological level. In biological systems, selection forces would take advantage of emergent patterns. This article is part of the theme issue ‘Unifying the essential concepts of biological networks: biological insights and philosophical foundations’.


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