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71.
72.
The sequences of the linked alpha 2- and alpha 1-globin genes of the equine
BI and BII haplotypes are greater than 99% identical within a 1.2-kb region
extending from approximately 75 bp upstream of the putative cap site to a
point approximately 150 bp 3' to the poly A addition signal. Differences
between the alpha 2 and alpha 1 genes that are common to both haplotypes
indicate that a major gene conversion occurred approximately 12 Myr ago and
that this has been followed by shorter, more localized, conversions.
Interhaplotype (allelic) comparisons at the alpha loci suggest that the BI
and BII haplotypes have probably existed independently greater than or
equal to 0.5 Myr and that the alpha 1 genes may have undergone a recent
interchromosomal gene conversion.
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73.
Kathryn Wright Kumudika de Silva Karren M. Plain Auriol C. Purdie Tamika A. Blair Iain G. Duggin Warwick J. Britton Stefan H. Oehlers 《PLoS pathogens》2021,17(4)
Pathogenic mycobacteria actively dysregulate protective host immune signalling pathways during infection to drive the formation of permissive granuloma microenvironments. Dynamic regulation of host microRNA (miRNA) expression is a conserved feature of mycobacterial infections across host-pathogen pairings. Here we examine the role of miR-206 in the zebrafish model of Mycobacterium marinum infection, which allows investigation of the early stages of granuloma formation. We find miR-206 is upregulated following infection by pathogenic M. marinum and that antagomir-mediated knockdown of miR-206 is protective against infection. We observed striking upregulation of cxcl12a and cxcr4b in infected miR-206 knockdown zebrafish embryos and live imaging revealed enhanced recruitment of neutrophils to sites of infection. We used CRISPR/Cas9-mediated knockdown of cxcl12a and cxcr4b expression and AMD3100 inhibition of Cxcr4 to show that the enhanced neutrophil response and reduced bacterial burden caused by miR-206 knockdown was dependent on the Cxcl12/Cxcr4 signalling axis. Together, our data illustrate a pathway through which pathogenic mycobacteria induce host miR-206 expression to suppress Cxcl12/Cxcr4 signalling and prevent protective neutrophil recruitment to granulomas. 相似文献
74.