September 2014 archive

Related Articles
Connecting alveolate cell biology with trophic ecology in the marine plankton using the ciliate Favella as a model.
FEMS Microbiol Ecol. 2014 Jul 19;
Authors: Echevarria ML, Wolfe GV, Strom SL, Tay…

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Assessing Symbiodinium diversity in scleractinian corals via next-generation sequencing-based genotyping of the ITS2 rDNA region.
Mol Ecol. 2014 Sep;23(17):4418-33
Authors: Arif C, Daniels C, Bayer…

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Are Niemann-Pick type C proteins key players in cnidarian-dinoflagellate endosymbioses?

Mol Ecol. 2014 Sep;23(18):4527-40

Authors: Dani V, Ganot P, Priouzeau F, Furla P, Sabourault C

Abstract
The symbiotic interaction between cnidarians, such as corals and sea anemones, and the unicellular algae Symbiodinium is regulated by yet poorly understood cellular mechanisms, despite the ecological importance of coral reefs. These mechanisms, including host-symbiont recognition and metabolic exchange, control symbiosis stability under normal conditions, but also lead to symbiosis breakdown (bleaching) during stress. This study describes the repertoire of the sterol-trafficking proteins Niemann-Pick type C (NPC1 and NPC2) in the symbiotic sea anemone Anemonia viridis. We found one NPC1 gene in contrast to the two genes (NPC1 and NPC1L1) present in vertebrate genomes. While only one NPC2 gene is present in many metazoans, this gene has been duplicated in cnidarians, and we detected four NPC2 genes in A. viridis. However, only one gene (AvNPC2-d) was upregulated in symbiotic relative to aposymbiotic sea anemones and displayed higher expression in the gastrodermis (symbiont-containing tissue) than in the epidermis. We performed immunolabelling experiments on tentacle cross sections and demonstrated that the AvNPC2-d protein was closely associated with symbiosomes. In addition, AvNPC1 and AvNPC2-d gene expression was strongly downregulated during stress. These data suggest that AvNPC2-d is involved in both the stability and dysfunction of cnidarian-dinoflagellate symbioses.

PMID: 25066219 [PubMed – in process]

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A genomic approach to coral-dinoflagellate symbiosis: studies of Acropora digitifera and Symbiodinium minutum.
Front Microbiol. 2014;5:336
Authors: Shinzato C, Mungpakdee S, Satoh N, Shoguchi E
…

Genomic Insights in Processes Driving the Infection of Alexandrium tamarense by the Parasitoid Amoebophrya sp.

Eukaryot Cell. 2014 Sep 19;

Authors: Lu Y, Wohlrab S, Glöckner G, Guillou L, John U

Abstract
The regulatory circuits during infection of dinoflagellates by their parasites are largely unknown on the molecular level. Here we provide molecular insights into these infection dynamics. Alexandrium tamarense is one of the most prominent Harmful Algal Bloom dinoflagellate. Its pathogen, the dinoflagellate parasitoid Amoebophrya spp., has been observed to infect and control the blooms of this species. We generated a dataset of transcripts from three time points during the infection of this parasite-host system (0, 6 and 96 hours). Assembly of all transcript data from the parasitoid (>900.000 reads/313MBp with 454/Roche NGS) yielded 14,455 contigs, to which we mapped the raw transcript reads of each time point of the infection cycle. We show that particular surface lectins are expressed at the beginning of the infection cycle, which likely mediate the attachment to the host cell. In a later phase signal transduction related genes together with transmembrane transport and cytoskeleton proteins point to a high integration of processes involved in host recognition, adhesion, and invasion. At the final maturation stage, cell division and proliferation related genes were highly expressed, reflecting the fast cell growth and nuclear division of the parasitoid. Our molecular insights in dinoflagellate parasitoid interaction point to general mechanisms also known from other eukaryotic parasites, especially from the Alveolata. These similarities indicate the presence of fundamental processes of parasitoid infection that have remained stable throughout evolution within different phyla.

PMID: 25239978 [PubMed – as supplied by publisher]