Biology subjects

Jivaji, A. M.

Publications and source records attributed to Jivaji, A. M..

4 recordsLinked to original sources

bioRxiv2026

Bloom-forming bacteria heavily invest in anti-phage defense

Bacterial blooms are characterized by unusually high cell densities and exceptionally low diversity and can profoundly alter ecosystem function and services. Bacteriophages have long been considered an important cause of mortality in blooms, acting as a mechanism for control. Here, we characterize the viral ecology of a long-lasting estuarine bloom of green sulfur bacteria (Chlorobiota). We combined direct cell and viral counts with metagenomic and metaproteomic data to characterize host and phage activity at different time points. The abundance of virus-like particles (VLPs) decreased at high cell densities, suggesting reduced lytic infection rates. The dominant organism, GSB-TRL01 (genus Prosthecochloris), apparently contained a large conjugative plasmid encoding five different anti-phage defense systems. The organism's genome encoded 13 additional defense systems. Compared to the average of five defense systems per microbial genome, this enrichment suggests robust anti-phage defense capabilities. Proteins from ten different defense systems on GSB-TRL01's genome and four systems from the conjugative plasmid were expressed in the proteome. This suggests that GSB-TRL01 invests heavily in anti-phage defense, leading to reduced lysis at high cell densities and allowing blooms to persist for weeks to months. To determine whether this ability is widespread among bloom forming organisms, we compared genomes of putative bloomers to those of non-blooming organisms. We found that bloomer genomes were significantly enriched with anti-phage defense systems. This challenges traditional paradigms of phage ecology in bloom-forming systems and suggests that microbes adapted to high-density growth may have evolved mechanisms to reduce their susceptibility to phage attack.

microbiology↗

bioRxiv2026

Mimicin, an antimicrobial protein encoded by mimivirus

Antimicrobial peptides (AMPs) are innate defense molecules found in all domains of life. Giant viruses of amoeba are known to thrive among complex microbial relationships within its hosts cells, hinting at the existence of virus-derived antimicrobial strategies. Here we show that viruses belonging to the Mimiviridae and Marseilleviridae families contain a higher density of in silico predicted AMPs per genome size than other viruses of amoeba. The investigation of potential AMPs led to the description of Mimicin, a taxonomically restricted 74 amino acid long protein coded by few mimiviruses. Mimicin contains three smaller predicted AMP sequences within it and has a broad in vitro antimicrobial activity against different bacteria, a yeast and two non-enveloped phages. In contrast, it has no activity against a marseillevirus, a mimivirus or human cell lines. When tested against bacterial endosymbionts co-cultured with Acanthamoeba terricola, Mimicin and its SIM-31 portion were able to control the attenuated Protochlamydia amoebophila but not the highly virulent Parachlamydia acanthamoebae. Based on deposited transcriptomic data, Mimicin is coded by an early gene more active during the beginning of the infection process. No structure could be predicted using Alphafold, while additional structural analysis indicate that Mimicin could be a highly disordered protein. In conclusion, we describe evidence of a biologically relevant antimicrobial activity derived from a giant virus. Mimicin highlights the relevance of AMPs from giant viruses for microbial ecology and opens the way for investigating their biotechnological and clinical potential.

microbiology↗

bioRxiv2025

Giant endogenous viral elements in the genome of the model protist Euglena gracilis reveal past interactions with giant viruses

Giant viruses in the phylum Nucleocytoviricota have increasingly been found integrated into the genomes of diverse eukaryotes. Here we report 8 Giant Endogenous Viral Elements (GEVEs) in the genome of the microalgae Euglena gracilis. The GEVEs bear signatures of genomic erosion, including invasion of transposable elements and duplications, suggesting that they are incapable of reactivation and virion production. Most of the GEVEs exhibit high average amino acid identity and cluster near each other in phylogenies of viral marker genes, suggesting that they are derived from the same initial viral lineage. Phylogenetic analysis of nucleocytovirus marker proteins reveals the viruses belong to the order Asfuvirales in the same broader lineage that includes African swine fever virus (ASFV), abalone asfarvirus (AbalV), and GEVEs recently found in the fungus Rhizophagus irregularis and the marine gastropod Elysia marginata, suggesting that widespread host range transitions have occurred in this lineage. This work expands the diversity of known endogenous giant viruses and expands the host range of the Asfuvirales to include the superkingdom Discoba.

bioinformatics↗

bioRxiv2024

Latent infection of an active giant endogenous virus in a unicellular green alga

Latency is a common strategy in a wide range of viral lineages, but its prevalence in giant viruses remains unknown. Here we describe the activity and viral production from a 617 kbp integrated giant viral element in the model green alga Chlamydomonas reinhardtii. We resolve the integrated viral region using long-read sequencing and show that viral particles are produced and released in otherwise healthy cultures. A diverse array of viral-encoded selfish genetic elements are expressed during GEVE reactivation and produce proteins that are packaged in virions. In addition, we show that field isolates of Chlamydomonas sp. harbor latent giant viruses related to the C. reinhardtii GEVE that exhibit similar infection dynamics, demonstrating that giant virus latency is prevalent in natural host communities. Our work reports the largest temperate virus documented to date and the first active GEVE identified in a unicellular eukaryote, substantially expanding the known limits of viral latency.

microbiology↗