February 2015 archive

Feb 27

Factors mediating plastid dependency and the origins of parasitism in apicomplexans and their close relatives.

Factors mediating plastid dependency and the origins of parasitism in apicomplexans and their close relatives.

Proc Natl Acad Sci U S A. 2015 Feb 25;

Authors: Janouškovec J, Tikhonenkov DV, Burki F, Howe AT, Kolísko M, Mylnikov AP, Keeling PJ

Abstract
Apicomplexans are a major lineage of parasites, including causative agents of malaria and toxoplasmosis. How such highly adapted parasites evolved from free-living ancestors is poorly understood, particularly because they contain nonphotosynthetic plastids with which they have a complex metabolic dependency. Here, we examine the origin of apicomplexan parasitism by resolving the evolutionary distribution of several key characteristics in their closest free-living relatives, photosynthetic chromerids and predatory colpodellids. Using environmental sequence data, we describe the diversity of these apicomplexan-related lineages and select five species that represent this diversity for transcriptome sequencing. Phylogenomic analysis recovered a monophyletic lineage of chromerids and colpodellids as the sister group to apicomplexans, and a complex distribution of retention versus loss for photosynthesis, plastid genomes, and plastid organelles. Reconstructing the evolution of all plastid and cytosolic metabolic pathways related to apicomplexan plastid function revealed an ancient dependency on plastid isoprenoid biosynthesis, predating the divergence of apicomplexan and dinoflagellates. Similarly, plastid genome retention is strongly linked to the retention of two genes in the plastid genome, sufB and clpC, altogether suggesting a relatively simple model for plastid retention and loss. Lastly, we examine the broader distribution of a suite of molecular characteristics previously linked to the origins of apicomplexan parasitism and find that virtually all are present in their free-living relatives. The emergence of parasitism may not be driven by acquisition of novel components, but rather by loss and modification of the existing, conserved traits.

PMID: 25717057 [PubMed – as supplied by publisher]

Feb 26

Metagenomic characterisation of viral communities in corals: Mining biological signal from methodological noise.

Metagenomic characterisation of viral communities in corals: Mining biological signal from methodological noise.
Environ Microbiol. 2015 Feb 24;
Authors: Wood-Charlson EM, Weynberg KD, Suttle CA, Roux S, van Oppen…

Feb 20

Whole-genome scans provide evidence of adaptive evolution in Malawian Plasmodium falciparum isolates.

Related Articles

Whole-genome scans provide evidence of adaptive evolution in Malawian Plasmodium falciparum isolates.

J Infect Dis. 2014 Dec 15;210(12):1991-2000

Authors: Ocholla H, Preston MD, Mipando M, Jensen AT, Campino S, MacInnis B, Alcock D, Terlouw A, Zongo I, Oudraogo JB, Djimde AA, Assefa S, Doumbo OK, Borrmann S, Nzila A, Marsh K, Fairhurst RM, Nosten F, Anderson TJ, Kwiatkowski DP, Craig A, Clark TG, Montgomery J

Abstract
BACKGROUND: Selection by host immunity and antimalarial drugs has driven extensive adaptive evolution in Plasmodium falciparum and continues to produce ever-changing landscapes of genetic variation.
METHODS: We performed whole-genome sequencing of 69 P. falciparum isolates from Malawi and used population genetics approaches to investigate genetic diversity and population structure and identify loci under selection.
RESULTS: High genetic diversity (π = 2.4 × 10(-4)), moderately high multiplicity of infection (2.7), and low linkage disequilibrium (500-bp) were observed in Chikhwawa District, Malawi, an area of high malaria transmission. Allele frequency-based tests provided evidence of recent population growth in Malawi and detected potential targets of host immunity and candidate vaccine antigens. Comparison of the sequence variation between isolates from Malawi and those from 5 geographically dispersed countries (Kenya, Burkina Faso, Mali, Cambodia, and Thailand) detected population genetic differences between Africa and Asia, within Southeast Asia, and within Africa. Haplotype-based tests of selection to sequence data from all 6 populations identified signals of directional selection at known drug-resistance loci, including pfcrt, pfdhps, pfmdr1, and pfgch1.
CONCLUSIONS: The sequence variations observed at drug-resistance loci reflect differences in each country’s historical use of antimalarial drugs and may be useful in formulating local malaria treatment guidelines.

PMID: 24948693 [PubMed – indexed for MEDLINE]

Feb 17

Metagenomic characterisation of viral communities in corals: Mining biological signal from methodological noise.

Related Articles
Metagenomic characterisation of viral communities in corals: Mining biological signal from methodological noise.
Environ Microbiol Rep. 2015 Feb 13;
Authors: Wood-Charlson EM, Weynberg KD, Suttle CA…

Feb 12

Divergent mitochondrial respiratory chains in phototrophic relatives of apicomplexan parasites.

Related Articles

Divergent mitochondrial respiratory chains in phototrophic relatives of apicomplexan parasites.

Mol Biol Evol. 2015 Feb 6;

Authors: Flegontov P, Michálek J, Janouškovec J, Lai H, Jirků M, Hajdušková E, Tomčala A, Otto TD, Keeling PJ, Pain A, Oborník M, Lukeš J

Abstract
Four respiratory complexes and ATP-synthase represent central functional units in mitochondria. In some mitochondria and derived anaerobic organelles, a few or all of these respiratory complexes have been lost during evolution. We show that the respiratory chain of Chromera velia, a phototrophic relative of parasitic apicomplexans, lacks complexes I and III, making it a uniquely reduced aerobic mitochondrion. In Chromera, putative lactate:cytochrome c oxidoreductases are predicted to transfer electrons from lactate to cytochrome c, rendering complex III unnecessary. The mitochondrial genome of Chromera has the smallest known protein-coding capacity of all mitochondria, encoding just cox1 and cox3 on heterogeneous linear molecules. In contrast, another photosynthetic relative of apicomplexans, Vitrella brassicaformis, retains the same set of genes as apicomplexans and dinoflagellates (cox1, cox3 and cob).

PMID: 25660376 [PubMed – as supplied by publisher]

Feb 11

Origin of robustness in generating drug-resistant malaria parasites.

Related Articles

Origin of robustness in generating drug-resistant malaria parasites.

Mol Biol Evol. 2014 Jul;31(7):1649-60

Authors: Kümpornsin K, Modchang C, Heinberg A, Ekland EH, Jirawatcharadech P, Chobson P, Suwanakitti N, Chaotheing S, Wilairat P, Deitsch KW, Kamchonwongpaisan S, Fidock DA, Kirkman LA, Yuthavong Y, Chookajorn T

Abstract
Biological robustness allows mutations to accumulate while maintaining functional phenotypes. Despite its crucial role in evolutionary processes, the mechanistic details of how robustness originates remain elusive. Using an evolutionary trajectory analysis approach, we demonstrate how robustness evolved in malaria parasites under selective pressure from an antimalarial drug inhibiting the folate synthesis pathway. A series of four nonsynonymous amino acid substitutions at the targeted enzyme, dihydrofolate reductase (DHFR), render the parasites highly resistant to the antifolate drug pyrimethamine. Nevertheless, the stepwise gain of these four dhfr mutations results in tradeoffs between pyrimethamine resistance and parasite fitness. Here, we report the epistatic interaction between dhfr mutations and amplification of the gene encoding the first upstream enzyme in the folate pathway, GTP cyclohydrolase I (GCH1). gch1 amplification confers low level pyrimethamine resistance and would thus be selected for by pyrimethamine treatment. Interestingly, the gch1 amplification can then be co-opted by the parasites because it reduces the cost of acquiring drug-resistant dhfr mutations downstream in the same metabolic pathway. The compensation of compromised fitness by extra GCH1 is an example of how robustness can evolve in a system and thus expand the accessibility of evolutionary trajectories leading toward highly resistant alleles. The evolution of robustness during the gain of drug-resistant mutations has broad implications for both the development of new drugs and molecular surveillance for resistance to existing drugs.

PMID: 24739308 [PubMed – indexed for MEDLINE]