@article{11344,
  abstract     = {Until recently, Shigella and enteroinvasive Escherichia coli were thought to be primate-restricted pathogens. The base of their pathogenicity is the type 3 secretion system (T3SS) encoded by the pINV virulence plasmid, which facilitates host cell invasion and subsequent proliferation. A large family of T3SS effectors, E3 ubiquitin-ligases encoded by the ipaH genes, have a key role in the Shigella pathogenicity through the modulation of cellular ubiquitination that degrades host proteins. However, recent genomic studies identified ipaH genes in the genomes of Escherichia marmotae, a potential marmot pathogen, and an E. coli extracted from fecal samples of bovine calves, suggesting that non-human hosts may also be infected by these strains, potentially pathogenic to humans. We performed a comparative genomic study of the functional repertoires in the ipaH gene family in Shigella and enteroinvasive Escherichia from human and predicted non-human hosts. We found that fewer than half of Shigella genomes had a complete set of ipaH genes, with frequent gene losses and duplications that were not consistent with the species tree and nomenclature. Non-human host IpaH proteins had a diverse set of substrate-binding domains and, in contrast to the Shigella proteins, two variants of the NEL C-terminal domain. Inconsistencies between strains phylogeny and composition of effectors indicate horizontal gene transfer between E. coli adapted to different hosts. These results provide a framework for understanding of ipaH-mediated host-pathogens interactions and suggest a need for a genomic study of fecal samples from diseased animals.},
  author       = {Dranenko, NO and Tutukina, MN and Gelfand, MS and Kondrashov, Fyodor and Bochkareva, Olga},
  issn         = {2045-2322},
  journal      = {Scientific Reports},
  publisher    = {Springer Nature},
  title        = {{Chromosome-encoded IpaH ubiquitin ligases indicate non-human enteroinvasive Escherichia}},
  doi          = {10.1038/s41598-022-10827-3},
  volume       = {12},
  year         = {2022},
}

@article{11447,
  abstract     = {Empirical essays of fitness landscapes suggest that they may be rugged, that is having multiple fitness peaks. Such fitness landscapes, those that have multiple peaks, necessarily have special local structures, called reciprocal sign epistasis (Poelwijk et al. in J Theor Biol 272:141–144, 2011). Here, we investigate the quantitative relationship between the number of fitness peaks and the number of reciprocal sign epistatic interactions. Previously, it has been shown (Poelwijk et al. in J Theor Biol 272:141–144, 2011) that pairwise reciprocal sign epistasis is a necessary but not sufficient condition for the existence of multiple peaks. Applying discrete Morse theory, which to our knowledge has never been used in this context, we extend this result by giving the minimal number of reciprocal sign epistatic interactions required to create a given number of peaks.},
  author       = {Saona Urmeneta, Raimundo J and Kondrashov, Fyodor and Khudiakova, Kseniia},
  issn         = {1522-9602},
  journal      = {Bulletin of Mathematical Biology},
  keywords     = {Computational Theory and Mathematics, General Agricultural and Biological Sciences, Pharmacology, General Environmental Science, General Biochemistry, Genetics and Molecular Biology, General Mathematics, Immunology, General Neuroscience},
  number       = {8},
  publisher    = {Springer Nature},
  title        = {{Relation between the number of peaks and the number of reciprocal sign epistatic interactions}},
  doi          = {10.1007/s11538-022-01029-z},
  volume       = {84},
  year         = {2022},
}