Superorganisms of the protist kingdom : a new level of biological organization

The concept of superorganism has a mixed reputation in biology-for some it is a convenient way of discussing supra-organismal levels of organization, and for others, little more than a poetic metaphor. Here, I show that a considerable step forward in the understanding of superorganisms results from a thorough review of the supra-organismal levels of organization now known to exist among the “unicellular” protists. Limiting the discussion to protists has enormous advantages: their bodies are very well studied and relatively simple (as compared to humans or termites, two standard examples in most discussions about superorganisms), and they exhibit an enormous diversity of anatomies and lifestyles. This allows for unprecedented resolution in describing forms of supra-organismal organization. Here, four criteria are used to differentiate loose, incidental associations of hosts with their microbiota from “actual” superorganisms: (1) obligatory character, (2) specific spatial localization of microbiota, (3) presence of attachment structures and (4) signs of co-evolution in phylogenetic analyses. Three groups-that have never before been described in the philosophical literature-merit special attention: Symbiontida (also called Postgaardea), Oxymonadida and Parabasalia. Specifically, it is argued that in certain cases-for Bihospites bacati and Calkinsia aureus (symbiontids), Streblomastix strix (an oxymonad), Joenia annectens and Mixotricha paradoxa (parabasalids) and Kentrophoros (a ciliate)-it is fully appropriate to describe the whole protist-microbiota assocation as a single organism (“superorganism”) and its elements as “tissues” or, arguably, even “organs”. To account for this level of biological complexity, I propose the term “structured superorganism”

Strain-dependent host transcriptional responses to toxoplasma infection are largely conserved in mammalian and avian hosts

Toxoplasma gondii has a remarkable ability to infect an enormous variety of mammalian and avian species. Given this, it is surprising that three strains (Types I/II/III) account for the majority of isolates from Europe/North America. The selective pressures that have driven the emergence of these particular strains, however, remain enigmatic. We hypothesized that strain selection might be partially driven by adaptation of strains for mammalian versus avian hosts. To test this, we examine in vitro, strain-dependent host responses in fibroblasts of a representative avian host, the chicken (Gallus gallus). Using gene expression profiling of infected chicken embryonic fibroblasts and pathway analysis to assess host response, we show here that chicken cells respond with distinct transcriptional profiles upon infection with Type II versus III strains that are reminiscent of profiles observed in mammalian cells. To identify the parasite drivers of these differences, chicken fibroblasts were infected with individual F1 progeny of a Type II x III cross and host gene expression was assessed for each by microarray. QTL mapping of transcriptional differences suggested, and deletion strains confirmed, that, as in mammalian cells, the polymorphic rhoptry kinase ROP16 is the major driver of strain-specific responses. We originally hypothesized that comparing avian versus mammalian host response might reveal an inversion in parasite strain-dependent phenotypes; specifically, for polymorphic effectors like ROP16, we hypothesized that the allele with most activity in mammalian cells might be less active in avian cells. Instead, we found that activity of ROP16 alleles appears to be conserved across host species; moreover, additional parasite loci that were previously mapped for strain-specific effects on mammalian response showed similar strain-specific effects in chicken cells. These results indicate that if different hosts select for different parasite genotypes, the selection operates downstream of the signaling occurring during the beginning of the host's immune response. © 2011 Ong et al

A bovine lymphosarcoma cell line infected with theileria annulata exhibits an irreversible reconfiguration of host cell gene expression

Theileria annulata, an intracellular parasite of bovine lymphoid cells, induces substantial phenotypic alterations to its host cell including continuous proliferation, cytoskeletal changes and resistance to apoptosis. While parasite induced modulation of host cell signal transduction pathways and NFκB activation are established, there remains considerable speculation on the complexities of the parasite directed control mechanisms that govern these radical changes to the host cell. Our objectives in this study were to provide a comprehensive analysis of the global changes to host cell gene expression with emphasis on those that result from direct intervention by the parasite. By using comparative microarray analysis of an uninfected bovine cell line and its Theileria infected counterpart, in conjunction with use of the specific parasitacidal agent, buparvaquone, we have identified a large number of host cell gene expression changes that result from parasite infection. Our results indicate that the viable parasite can irreversibly modify the transformed phenotype of a bovine cell line. Fifty percent of genes with altered expression failed to show a reversible response to parasite death, a possible contributing factor to initiation of host cell apoptosis. The genes that did show an early predicted response to loss of parasite viability highlighted a sub-group of genes that are likely to be under direct control by parasite infection. Network and pathway analysis demonstrated that this sub-group is significantly enriched for genes involved in regulation of chromatin modification and gene expression. The results provide evidence that the Theileria parasite has the regulatory capacity to generate widespread change to host cell gene expression in a complex and largely irreversible manner

Auditory Physiology

Contains reports on one research projects split into ten sections.National Institutes of Health (Grant 5 P01 NS13126)National Institutes of Health (Grant 5 RO1 NS18682)National Institutes of Health (Grant 5 RO1 NS20322)National Institutes of Health (Grant 5 RO1 NS20269)National Institutes of Health (Grant 5 PO1 NS23734)National Institutes of Health (Grant 5 T32 NS07047)Symbion, Inc

Signal Transmission in the Auditory System

Contains table of contents for Section 3, an introduction, and reports on seven research projects.National Institutes of Health Grant 5 R01 DC00194National Institutes of Health Grant P01 DC00119National Institutes of Health Grant F32 DC00073National Institutes of Health Grant 5 R01 DC00473National Institutes of Health Grant 2 R01 DC00238National Institutes of Health Grant 2 R01 DC00235National Institutes of Health Grant 5 P01 DC00361National Institutes of Health Grant T32 DC00006Whitaker Health Sciences Fun

Transcriptional Analysis of Murine Macrophages Infected with Different Toxoplasma Strains Identifies Novel Regulation of Host Signaling Pathways

Most isolates of Toxoplasma from Europe and North America fall into one of three genetically distinct clonal lineages, the type I, II and III lineages. However, in South America these strains are rarely isolated and instead a great variety of other strains are found. T. gondii strains differ widely in a number of phenotypes in mice, such as virulence, persistence, oral infectivity, migratory capacity, induction of cytokine expression and modulation of host gene expression. The outcome of toxoplasmosis in patients is also variable and we hypothesize that, besides host and environmental factors, the genotype of the parasite strain plays a major role. The molecular basis for these differences in pathogenesis, especially in strains other than the clonal lineages, remains largely unexplored. Macrophages play an essential role in the early immune response against T. gondii and are also the cell type preferentially infected in vivo. To determine if non-canonical Toxoplasma strains have unique interactions with the host cell, we infected murine macrophages with 29 different Toxoplasma strains, representing global diversity, and used RNA-sequencing to determine host and parasite transcriptomes. We identified large differences between strains in the expression level of known parasite effectors and large chromosomal structural variation in some strains. We also identified novel strain-specifically regulated host pathways, including the regulation of the type I interferon response by some atypical strains. IFNβ production by infected cells was associated with parasite killing, independent of interferon gamma activation, and dependent on endosomal Toll-like receptors in macrophages and the cytoplasmic receptor retinoic acid-inducible gene 1 (RIG-I) in fibroblasts.National Institutes of Health (U.S.) (R01-AI080621)New England Regional Center of Excellence for Biodefense and Emerging Infectious Diseases (Developmental Grant AIO57159)Pew Charitable Trusts (Biomedical Scholars Program)Robert A. Swanson Career Development awardThe Knights Templar Eye Foundation, Inc.Pre-Doctoral Grant in the Biological Sciences (5-T32-GM007287-33)Cleo and Paul Schimmel Foundatio

Signal Transmission in the Auditory System

Contains table of contents for Section 3 and reports on nine research projects.National Institutes of Health (Grant 5 P01 NS13126)National Institutes of Health (Grant 5 P01 NS23734)National Institutes of Health (Grant 5 R01 NS18682)National Institutes of Health (Grant 5 RO1 NS25995)National Institutes of Health (Grant 5 R01 NS20269)National Institutes of Health (Grant 5 R01 NS20322)National Institutes of Health (Grant 5 T32 NS07047)Johnson and Johnson Foundatio

Signal Transmission in the Auditory System

Contains table of contents for Section 3, an introduction and reports on six research projects.Health Sciences FundNational Institutes of Health Grant 5 R01 DC00194National Institutes of Health Grant 8 P01 DC00119National Institutes of Health Grant 5 R01 DC00473National Institutes of Health Grant 5 R01 DC00238National Institutes of Health Grant 5 T32 DC00006National Institutes of Health Grant 5 P01 DC00361National Institutes of Health Grant 5 R01 DC00235Peoples Republic of China FellowshipUnisys Corporation Doctoral FellowshipWhitaker Health Sciences Fellowshi

Signal Transmission in the Auditory System

Contains table of contents for Section 3, an introduction and reports on six research projects.National Institutes of Health Grant R01-DC-00194National Institutes of Health Contract P01-DC-00119National Institutes of Health Fellowship F32-DC00073National Institutes of Health Grant R01-DC00238National Institutes of Health Grant R01-DC00473National Institutes of Health Grant T32-DC00006National Institutes of Health Grant T32-DC00038National Institutes of Health Contract P01-DC00361National Institutes of Health Grant R01-DC00235National Institutes of Health Contract N01-DC2240

Signal Transmission in the Auditory System

Contains table of contents for Section 3, an introduction and reports on nine research projects.National Institutes of Health Grant 5 T32 NS07047National Institutes of Health Grant 5 P01 NS13126National Institutes of Health Grant 8 R01 DC00194National Institutes of Health Grant 5 R01 NS25995National Institutes of Health Grant 8 R01 DC00238National Institutes of Health Grant 5 R01 NS20322National Institutes of Health Grant 5 R01 DC00235National Institutes of Health Grant 5 R01 NS20269National Institutes of Health Grant 1 P01 NS23734Johnson and Johnson FoundationUnisys Corporation Doctoral Fellowshi