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Based on models of host-pathogen coevolution, resistance is commonly predicted to involve multiple host genes and strong interactions between alleles at different host loci.
We specifically concentrated on nested gene arrangements because the highly conserved structures of the host loci allow a more reliable identification of orthologous genes.
To our knowledge, an investigation of the impact of retroviral integration on nuclear positioning of the host loci by a comparison to the same loci without integration was not previously performed.
When the number of host loci is increased at the lower parasite mutation rate used in Figure 4 (10-3), there is a small difference in maximum adaptation scores between clonal and sexual populations that is consistent.
On the host side, work has uncovered a number of host factors crucial for mycobacterial recognition and growth, and ongoing screening efforts continue to identify novel host loci involved in the process of infection.
These host loci were shown to control individual microbial species, groups of related taxa, or groups of distantly related microorganisms and contained genes involved in immune signaling, such as Irak3, Lyz1, Lyz2, Ifng, and Il22 [ 59].
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A diploid host locus encodes symbolically a defence protein with 32 × 1-bit sites (= 2 × 16-bit alleles).
An integrated retroviral DNA sequence of only a few kb in length thus altered large-scale chromatin structure of the host locus.
This, in turn, could have contributed to the imprinted expression at the host locus, involving allelic acquisition of DNA methylation at key regulatory sequences.
Thus the basic requirements for adaptation in our model were presence of loci in the host and worm that interact and genetic variation in both the worm and host locus.
It is assumed that the regulatory elements of a nested gene are dispersed throughout the host locus and that selection is acting to preserve a particular mode of gene regulation (Tsang et al. 2009).
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