Bioinformatics Analysis of Protein Homologues of Magnetotactic Bacteria Magnetosome Island Proteins in Human Proteome

Abstract

Background. The number of biogenic magnetic nanoparticles (BMN), present in human organs and tissues in the form of magnetite (ferrimagnetic iron oxide), increases in oncological and neurodegenerative diseases. Therefore, the study of homologues of BMN biomineralization proteins (mam-proteins) of magnetotaxis bacteria (MTB) in human proteome is relevant task. This concern is due primarily to the expediency of establishing patterns of changes in the expression of these proteins and searching for correlations with oncological and neurodegenerative diseases. Objective. We are aimed to conduct the bioinformatic analysis of homologues of MTB mam-proteins in humans and to determine the patterns of changes in the expression of these proteins, as well as to search for their connections with the specified diseases. This will allow to identify the main candidate proteins (among the known homologues of MTB mam-proteins in humans) for experimental verification of their participation in the genetically programmed mechanism of BMN biosynthesis in humans. Methods. The methods of comparative genomics were used, in particular the BLAST (Basic Local Alignment Search Tool) program of the NCBI database. Database tools were also used: NCBI Conserved Domain Search, The Cancer Genome Atlas database, Ensembl database. Results. The bioinformatic analysis of 16 homologues of MTB mam-proteins in humans was carried out, namely: PEX5, ANAPC7, CDC23, CDC27 and SGTA – homologues of MamA in MTB; SLC30A4, SLC30A9, SLC39A3 and SLC39A4 – homologs of MamB and MamM in MTB; HTRA1, HTRA2, HTRA3 and HTRA4 – MamO and MamE homologues in MTB; SCRIB, PDZK1 and PDZD3 – MamE homologues in MTB. Using pairwise alignments, the degree of homology between the mam-proteins of the MTB magnetosome island and the corresponding human proteins was determined, conserved domains and their functions were determined, changes in their expression levels in cancer and normal conditions were determined by analyzing the relevant databases, and the metabolic pathways to which the data proteins are involved were analysed. The analysis of the obtained data allowed to assume the presence of the main homologues of the MTB mam-proteins of the magnetosome island in humans, which cause an increase in the level of BMN in oncological and neurodegenerative diseases, namely: an increase in the expression level of the proteins PEX5, ANAPC7 (homologs of MamA), SLC39A3, SLC39A4 (homologs of MamB and MamM), HTRA4 (MamO and MamE homolog) and SCRIB (MamE homolog). Conclusions. The obtained data allow us to assume that the proteins PEX5, ANAPC7, SGTA, SLC39A3, SLC39A4, HTRA4 and SCRIB are the main homologues of the MTB mam-proteins in humans and cause an increase in the level of BMN in oncological and neurodegenerative diseases.