Shrink it or lose it: balancing loss of function with shrinking genomes in the microsporidia

Keeling, Patrick J.; Corradi, Nicolas

doi:10.4161/viru.2.1.14606

Cited by 34 publications

(27 citation statements)

References 24 publications

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“…Mitochondria have a bacterial type circular genome in multiple copies that is separate from but is coordinated with the nuclear genome [18, 19] but the number of mitochondrial genes is less than 1% of their proteome. Significant gene loss also occurs in obligate intracellular pathogens and symbionts and even descriptions of the minimum gene size needed by engineered bacteria are now being defined[20, 21]. Why the mitochondrial genome is even preserved at all is not clear, but the mitochondrial genome codes for 13 mRNA's that translate to membrane protein constituents of the respiratory chain as well as for the tRNA for a 12 S and 16S ribozyme and for 22 tRNAs [18].…”

Section: Introductionmentioning

confidence: 99%

Known unknowns of cardiolipin signaling: The best is yet to come

Maguire

Tyurina

Mohammadyani

et al. 2017

Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biolog

100

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Since its discovery 75 years ago, a wealth of knowledge has accumulated on the role of cardiolipin, the hallmark phospholipid of mitochondria, in bioenergetics and particularly on the structural organization of the inner mitochondrial membrane. A surge of interest in this anionic doubly-charged tetra-acylated lipid found in both prokaryotes and mitochondria has emerged based on its newly discovered signaling functions. Cardiolipin displays organ, tissue, cellular and transmembrane distribution asymmetries. A collapse of the membrane asymmetry represents a pro-mitophageal mechanism whereby externalized cardiolipin acts as an “eat-me” signal. Oxidation of cardiolipin's polyunsaturated acyl chains - catalyzed by cardiolipin complexes with cytochrome c. - is a pro-apoptotic signal. The messaging functions of myriads of cardiolipin species and their oxidation products are now being recognized as important intracellular and extracellular signals for innate and adaptive immune systems. This newly developing field of research exploring cardiolipin signaling is the main subject of this review.

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Section: Introductionmentioning

confidence: 99%

Known unknowns of cardiolipin signaling: The best is yet to come

Maguire

Tyurina

Mohammadyani

et al. 2017

Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biolog

100

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“…Genome analyses also show that all microsporidia have lost the pathways for oxidative phosphorylation and the tricarboxylic acid (TCA) cycle [5,6] and Enterocytozoon bieneusi , a major pathogen of immunocompromised patients, has also lost glycolysis [7]. So the capacity for independent biosynthesis of ATP appears to be very limited in microsporidia.…”

Section: Introductionmentioning

confidence: 99%

“…Host cells can make nucleotides via de novo biosynthesis and regenerate ATP by oxidative phosphorylation—these pathways are absent in microsporidia [5]. Host purine nucleotides can be stolen using microsporidia NTT transporters and then efficiently used and recycled by the parasites [18].…”

Section: Introductionmentioning

confidence: 99%

Microsporidia: Why Make Nucleotides if You Can Steal Them?

2016

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Microsporidia are strict obligate intracellular parasites that infect a wide range of eukaryotes including humans and economically important fish and insects. Surviving and flourishing inside another eukaryotic cell is a very specialised lifestyle that requires evolutionary innovation. Genome sequence analyses show that microsporidia have lost most of the genes needed for making primary metabolites, such as amino acids and nucleotides, and also that they have only a limited capacity for making adenosine triphosphate (ATP). Since microsporidia cannot grow and replicate without the enormous amounts of energy and nucleotide building blocks needed for protein, DNA, and RNA biosynthesis, they must have evolved ways of stealing these substrates from the infected host cell. Providing they can do this, genome analyses suggest that microsporidia have the enzyme repertoire needed to use and regenerate the imported nucleotides efficiently. Recent functional studies suggest that a critical innovation for adapting to intracellular life was the acquisition by lateral gene transfer of nucleotide transport (NTT) proteins that are now present in multiple copies in all microsporidian genomes. These proteins are expressed on the parasite surface and allow microsporidia to steal ATP and other purine nucleotides for energy and biosynthesis from their host. However, it remains unclear how other essential metabolites, such as pyrimidine nucleotides, are acquired. Transcriptomic and experimental studies suggest that microsporidia might manipulate host cell metabolism and cell biological processes to promote nucleotide synthesis and to maximise the potential for ATP and nucleotide import. In this review, we summarise recent genomic and functional data relating to how microsporidia exploit their hosts for energy and building blocks needed for growth and nucleic acid metabolism and we identify some remaining outstanding questions.

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“…Microsporidian genomes encode a greatly reduced metabolic potential compared with other eukaryotes (Keeling and Corradi 2011), yet these microbes can still undergo dramatic proliferation within host cells. This rapid growth likely places a substantial metabolic burden on the host to generate building blocks such as nucleotides, amino acids, and lipids, which are needed by the replicating parasite cells.…”

mentioning

confidence: 99%

Microsporidian genome analysis reveals evolutionary strategies for obligate intracellular growth

et al. 2012

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Microsporidia comprise a large phylum of obligate intracellular eukaryotes that are fungal-related parasites responsible for widespread disease, and here we address questions about microsporidia biology and evolution. We sequenced three microsporidian genomes from two species, Nematocida parisii and Nematocida sp1, which are natural pathogens of Caenorhabditis nematodes and provide model systems for studying microsporidian pathogenesis. We performed deep sequencing of transcripts from a time course of N. parisii infection. Examination of pathogen gene expression revealed compact transcripts and a dramatic takeover of host cells by Nematocida. We also performed phylogenomic analyses of Nematocida and other microsporidian genomes to refine microsporidian phylogeny and identify evolutionary events of gene loss, acquisition, and modification. In particular, we found that all microsporidia lost the tumor-suppressor gene retinoblastoma, which we speculate could accelerate the parasite cell cycle and increase the mutation rate. We also found that microsporidia acquired transporters that could import nucleosides to fuel rapid growth.

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Shrink it or lose it: balancing loss of function with shrinking genomes in the microsporidia

Cited by 34 publications

References 24 publications

Known unknowns of cardiolipin signaling: The best is yet to come

Known unknowns of cardiolipin signaling: The best is yet to come

Microsporidia: Why Make Nucleotides if You Can Steal Them?

Microsporidian genome analysis reveals evolutionary strategies for obligate intracellular growth

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