Although IL-1β is a proinflammatory cytokine, its effects on aneurysm formation and macrophage polarization differ from TNF-α. The differential effects of IL-1β and TNF-α inhibition are related to M1/M2 macrophage polarization and this may account for the differences in clinical efficacy of IL-1β and TNF-α antibody therapies in management of inflammatory diseases.
BackgroundThe formation of an allopolyploid is a two step process, comprising an initial wide hybridization event, which is later followed by a whole genome doubling. Both processes can affect the transcription of homoeologues. Here, RNA-Seq was used to obtain the genome-wide leaf transcriptome of two independent Triticum turgidum × Aegilops tauschii allotriploids (F1), along with their spontaneous allohexaploids (S1) and their parental lines. The resulting sequence data were then used to characterize variation in homoeologue transcript abundance.ResultsThe hybridization event strongly down-regulated D-subgenome homoeologues, but this effect was in many cases reversed by whole genome doubling. The suppression of D-subgenome homoeologue transcription resulted in a marked frequency of parental transcription level dominance, especially with respect to genes encoding proteins involved in photosynthesis. Singletons (genes where no homoeologues were present) were frequently transcribed at both the allotriploid and allohexaploid plants.ConclusionsThe implication is that whole genome doubling helps to overcome the phenotypic weakness of the allotriploid, restoring a more favourable gene dosage in genes experiencing transcription level dominance in hexaploid wheat.Electronic supplementary materialThe online version of this article (doi:10.1186/s12864-017-3558-0) contains supplementary material, which is available to authorized users.
Zika virus (ZIKV) is a neurotrophic flavivirus that is capable of infecting humans, leading to brain abnormalities during fetal development. The ZIKV infectivity in neural target cells remains poorly understood. Here, we found that ZIKV specifically infected glial fibrillary acidic protein- and S100B-positive primary human astrocytes derived from fetal brains. In contrast, neuron-specific Class III β-tubulin (TuJ1)-positive neurons in the astrocyte cultures and SOX2-positive neural progenitor cells derived from the fetal brains were less susceptible to ZIKV infection compared with astrocytes. The infected astrocytes released competent viral particles and manifested programmed cell death with a progressive cytopathic effect. Interestingly, ZIKV infection in human fetal astrocytes induced a significant increase of extracellular vesicles (EVs). Treatment with GW4869, a specific inhibitor of neutral sphingomyelinase-2, decreased EV levels, suppressed ZIKV propagation, and reduced the release of infectious virions in astrocytes. Therefore, ZIKV infects primary human fetal astrocytes and the infection can be suppressed by neutral sphingomyelinase-2 inhibitor GW4869. Further investigation into sphingomyelin metabolism and EVs may provide insights to the therapeutic treatment of ZIKV infection.
Powdery mildew, caused by the fungus Blumeria graminis f. sp. tritici, represents a yield constraint in many parts of the world. Here, the introduction of a resistance gene carried by the cereal rye cv. Qinling chromosome 6R was transferred into wheat in the form of spontaneous balanced translocation induced in plants doubly monosomic for chromosomes 6R and 6A. The translocation, along with other structural variants, was detected using in situ hybridization and genetic markers. The differential disease response of plants harboring various fragments of 6R indicated that a powdery mildew resistance gene(s) was present on both arms of rye chromosome 6R. Based on karyotyping, the short arm gene, designated Pm56, was mapped to the subtelomere region of the arm. The Robertsonian translocation 6AL⋅6RS can be exploited by wheat breeders as a novel resistance resource.
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