Biology subjects

Terenin, I.

Publications and source records attributed to Terenin, I..

3 recordsLinked to original sources

bioRxiv2026

Characterization of six environmental coli-phages isolated in Astana, Kazakhstan, during the School of Molecular and Theoretical Biology

Bacteriophage (phage) collections are essential resources for studying virus-host interactions in bacterial species. Here, we report six Escherichia coli-infecting phages that expand the Lund Collection of Bacteriophages. These phages were isolated in 2025 within the framework of the School of Molecular and Theoretical Biology for high-school students, from samples collected in Lake Taldykol, Astana, Kazakhstan, using E. coli strains MG1655{Delta}RM and EV36 as hosts. The isolated phages comprise Taldykol (LuPh6), a member of the genus Kagunavirus; Aidakhar (LuPh7) of the genus Phapecoctavirus; Samruk (LuPh8) of the genus Tequintavirus; the T-odd-like phage Baiterek (LuPh9) of the genus Vequintavirus; and two T-even-like phages Tulpar (LuPh10) and Shurale (LuPh11) that belong to the Tequatrovirus genus. This expanded phage collection enhances the toolkit for investigating phage-host interactions and their molecular mechanisms and highlights the use of phage isolation as a component of high school research education. ImportancePhage collections are a key resource for studying phage biology, phage-bacteria interactions and bacterial immune systems. Here, we extend the Lund Phage Collection through the isolation and characterisation of six E. coli-infecting phages, including three novel species (LuPh6, LuPh8 and LuPh11) as well as a member of the genus Phapecoctavirus that not represented in widely used collections such as BASEL (LuPh7). This study expands the resources available for probing phage-host interactions and demonstrates an example of integrating phage research into education of high school students.

microbiology↗

bioRxiv2026

Nucleoid-associated proteins sense phage-induced genome damage to elicit abortive infection

Bacteria have evolved diverse immune strategies to detect and neutralize bacteriophage infection. Here, we describe an unprecedented paradigm in which a chromosome-architecting nucleoid-associated protein (NAP) is repurposed as a viral infection sensor. When phage attack leads to genome degradation, the NAP sensor is released from the nucleoid to the cytoplasm, where it binds and activates diverse immune effectors. One such effector is a nucleotide-modifying toxin normally existing as an inactive homotetramer. NAP binding converts it into a catalytically active heterotrimer that halts both transcription and translation. Phylogenetic analyses unveiled the high modularity, polyphyletic origin, and wide distribution of NAP-mediated defenses. Collectively, we define a distinct class of defense systems in which bacteria sense phage-induced genome damage through NAP relocation, highlighting an unexpected but essential role for these proteins as sentinels of genome integrity.

microbiology↗

bioRxiv2021

Clinically observed deletions in SARS-CoV-2 Nsp1 affect protein stability and its ability to inhibit translation

Nonstructural protein 1 (Nsp1) is a major pathogenicity factor of SARS-CoV-2. It inhibits host-cell translation, primarily through a direct interaction between its C-terminal domain and the mRNA entry channel of the 40S small ribosomal subunit, with an N-terminal {beta}-barrel domain fine-tuning the inhibition and promoting selective translation of viral mRNA. SARS-CoV-2 nsp1 is a target of recurring deletions, some of which are associated with altered COVID-19 disease progression. To provide the biochemical basis for this, it is essential to characterize the efficiency of translational inhibition by the said protein variants. Here, we use an in vitro translation system to investigate the translation inhibition capacity of a series of clinically observed Nsp1 deletion variants. We find that a frequently observed deletion of residues 79-89 destabilized the N-terminal domain (NTD) and severely reduced the capacity of Nsp1 to inhibit translation. Interestingly, shorter deletions in the same region have been reported to effect the type I interferon response but did not affect translation inhibition, indicating a possible translation-independent role of the Nsp1 NTD in interferon response modulation. Taken together, our data provide a mechanistic basis for understanding how deletions in Nsp1 influence SARS-CoV-2 induction of interferon response and COVID-19 progression.

microbiology↗