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- Werren, John H, et al.
(författare)
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Functional and evolutionary insights from the genomes of three parasitoid Nasonia species.
- 2010
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Ingår i: Science. - : American Association for the Advancement of Science (AAAS). - 0036-8075 .- 1095-9203. ; 327:5963, s. 343-8
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Tidskriftsartikel (refereegranskat)abstract
- We report here genome sequences and comparative analyses of three closely related parasitoid wasps: Nasonia vitripennis, N. giraulti, and N. longicornis. Parasitoids are important regulators of arthropod populations, including major agricultural pests and disease vectors, and Nasonia is an emerging genetic model, particularly for evolutionary and developmental genetics. Key findings include the identification of a functional DNA methylation tool kit; hymenopteran-specific genes including diverse venoms; lateral gene transfers among Pox viruses, Wolbachia, and Nasonia; and the rapid evolution of genes involved in nuclear-mitochondrial interactions that are implicated in speciation. Newly developed genome resources advance Nasonia for genetic research, accelerate mapping and cloning of quantitative trait loci, and will ultimately provide tools and knowledge for further increasing the utility of parasitoids as pest insect-control agents.
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| 2. |
- Ahola, Virpi, et al.
(författare)
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The Glanville fritillary genome retains an ancient karyotype and reveals selective chromosomal fusions in Lepidoptera
- 2014
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Ingår i: Nature Communications. - : Springer Science and Business Media LLC. - 2041-1723. ; 5, s. 4737-
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Tidskriftsartikel (refereegranskat)abstract
- Previous studies have reported that chromosome synteny in Lepidoptera has been well conserved, yet the number of haploid chromosomes varies widely from 5 to 223. Here we report the genome (393 Mb) of the Glanville fritillary butterfly (Melitaea cinxia; Nymphalidae), a widely recognized model species in metapopulation biology and eco-evolutionary research, which has the putative ancestral karyotype of n = 31. Using a phylogenetic analyses of Nymphalidae and of other Lepidoptera, combined with orthologue-level comparisons of chromosomes, we conclude that the ancestral lepidopteran karyotype has been n = 31 for at least 140 My. We show that fusion chromosomes have retained the ancestral chromosome segments and very few rearrangements have occurred across the fusion sites. The same, shortest ancestral chromosomes have independently participated in fusion events in species with smaller karyotypes. The short chromosomes have higher rearrangement rate than long ones. These characteristics highlight distinctive features of the evolutionary dynamics of butterflies and moths.
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| 3. |
- Waterhouse, Christopher C M, et al.
(författare)
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Secretory cell hyperplasia and defects in Notch activity in a mouse model of leukocyte adhesion deficiency type II
- 2010
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Ingår i: Gastroenterology. - : Elsevier BV. - 0016-5085 .- 1528-0012. ; 138:3, s. 1079-1090.e5
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND & AIMS:Leukocyte adhesion deficiency II (LAD II) is a rare condition caused by defective protein fucosylation, causing decreased leukocyte rolling, psychomotor retardation, and poor growth. The ligand-binding activity of Notch, a gastrointestinal signaling protein, depends on O-fucosylation. We investigated Notch signaling and intestinal epithelial architecture in a mouse model of LAD II.METHODS:Mice lacking 3,5-epimerase/4-reductase (FX) or FX(-/-) bone marrow chimeras (with either wild-type or FX(-/-) bone marrow) were maintained on a fucose-free diet. Intestinal secretory epithelial cells were quantified by histology and immunohistochemistry. Reverse transcription-polymerase chain reaction and immunoblot analyses were used to detect Notch-regulated genes in isolated crypt epithelium. Intestinal leukocyte-endothelial interaction was quantified by intravital microscopy. The intestinal epithelium of 2-week-old FX(-/-) mice was transfected with an adenoviral vector expressing a constitutively active form of Notch.RESULTS: FX(-/-) mice rapidly exhibited secretory epithelial cell hyperplasia, reduced cell proliferation, and altered epithelial gene expression patterns consistent with reduced Notch signaling. These effects were reversed when mice were given dietary fucose or by adenoviral transfection of the intestinal epithelium with the Notch intracellular domain.CONCLUSIONS: In a mouse model of LAD II, secretory cell hyperplasia occurs in the small intestine and colon; these effects depend on Notch signaling. Defects in Notch signaling might therefore be involved in the pathogenesis of this rare pediatric condition.
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