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<p>There is ever more evidence that the manifestation of a variety of diseases may involve the network-based organization of genes with common regulatory elements affecting their expression. Our previous work identified 12 genes associated with neurodegenerative diseases (<i>kcne2</i>, <i>gart</i>, <i>tmem50b</i>, <i>il10rb</i>, <i>ifnar2</i>, <i>urb1</i>, <i>grik1</i>, <i>usp16</i>, <i>ltn1</i>, <i>cyyr1</i>, <i>app</i>, and <i>jam2</i>), which carry, within their introns, the product of recombination between the LINE1 and BovB retrotransposons with regions with homology to various microRNAs and characterized by high levels of evolutionary conservation of genetic linkage in mammals, including the platypus (chromosome 17) and humans (chromosome 21). With the aim of identifying possible functional relationships that might contribute to the preservation of the genetic linkage of these genes, we carried out an in silico analysis of specific functional features of their expression. This analysis showed that the proteins encoded by these genes take part in the fundamental biological processes of cellular life support and are closely related to each other. Thus, an excess of the <i>app</i> gene product reduces or blocks the processes underlying cell excitation. A decrease in cell excitability can, in turn, lead to inhibition of the expression of the genes encoding proteins involved in intercellular interactions, protein synthesis, purine synthesis, activation of cellular aging, and cell death, along with increases in the activity of anti-inflammatory processes. The results of this study suggest that the close linkage of the 12 genes under consideration may be maintained during evolution because of this relationship and the presence of identical regulatory network elements within them, introducing the possibility of synchronized adjustment of their expression. Thus, study of the synteny of genes closely associated with neuropathologies can contribute to a deeper understanding of the genetic mechanisms of regulation of higher nervous activity.</p>

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Genomics of Higher Nervous Activity: Evolutionary Conservation of Synteny of a Block of Genes Involved in Neuropathologies

  • 期刊论文

  • 发表日期：

    2025年7月1日

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  • G. Yu. Kosovsky,
  • O. I. Skobel,
  • T. T. Glazko

摘要

There is ever more evidence that the manifestation of a variety of diseases may involve the network-based organization of genes with common regulatory elements affecting their expression. Our previous work identified 12 genes associated with neurodegenerative diseases (kcne2, gart, tmem50b, il10rb, ifnar2, urb1, grik1, usp16, ltn1, cyyr1, app, and jam2), which carry, within their introns, the product of recombination between the LINE1 and BovB retrotransposons with regions with homology to various microRNAs and characterized by high levels of evolutionary conservation of genetic linkage in mammals, including the platypus (chromosome 17) and humans (chromosome 21). With the aim of identifying possible functional relationships that might contribute to the preservation of the genetic linkage of these genes, we carried out an in silico analysis of specific functional features of their expression. This analysis showed that the proteins encoded by these genes take part in the fundamental biological processes of cellular life support and are closely related to each other. Thus, an excess of the app gene product reduces or blocks the processes underlying cell excitation. A decrease in cell excitability can, in turn, lead to inhibition of the expression of the genes encoding proteins involved in intercellular interactions, protein synthesis, purine synthesis, activation of cellular aging, and cell death, along with increases in the activity of anti-inflammatory processes. The results of this study suggest that the close linkage of the 12 genes under consideration may be maintained during evolution because of this relationship and the presence of identical regulatory network elements within them, introducing the possibility of synchronized adjustment of their expression. Thus, study of the synteny of genes closely associated with neuropathologies can contribute to a deeper understanding of the genetic mechanisms of regulation of higher nervous activity.