Biology subjects

Lopez-Madrigal, S.

Publications and source records attributed to Lopez-Madrigal, S..

3 recordsLinked to original sources

bioRxiv2025

Nested Connections: Local Phage and Broad Plasmid Sharing in the Honey Bee Mobilome

Honey bees rely on bacterial symbionts for their nutritional needs and for protection against invading pathogens. Genetic diversity among strains within the colony has the potential to impact symbiont function and subsequently the benefits that honey bees receive from them. Mobilized genes vectored by mobile genetic elements (MGEs) like phages, transposons, conjugative elements and plasmids, are known to rapidly alter bacterial phenotypes. We identified phages and plasmids in genomes of the symbiont Bombella apis between two colonies, with the goal of understanding which MGEs contribute to strain diversification as well as MGE distribution across colonies and between microbial species. Interestingly, we found some B. apis strains carry plasmids while all harbor a diversity of integrated phages, with only one phage clusters conserved across all. Identified B. apis phages are not found outside of the Bombella and Saccaribacter species, suggesting some host specificity for these MGEs. Of the five plasmids discovered, two appear to be phage-plasmids with high similarity to phages found in previously sequenced B. apis genomes. Interestingly, three plasmids in B. apis shared significant average nucleotide identity with known plasmids from acetic acid bacteria isolated from flowers, plants, and fermented foods. This result suggests that B. apis has acquired MGEs, either vertically or horizontally, from plant- and fermented-food associated AABs. Overall, our findings suggest that MGE content varies between colonies and has the potential to shape genetic and phenotypic variation between strains.

microbiology↗

bioRxiv2025

Wolbachia uses ankyrin repeats to target specific fly proteins

Arthropods, the most diverse phylum on Earth, are hosts to a plethora of bacterial parasites that secrete various effectors of unknown function during infection. The most prevalent of these is the intracellular bacterium Wolbachia pipientis. The microbe infects between 40-60% of insect species, causes important reproductive manipulations, and limits virus replication in arthropod vectors, becoming a promising biocontrol agent. Understanding the molecular basis of Wolbachia infection and Wolbachia-induced phenotypes is critical to the use of Wolbachia in vector control. These Wolbachia ankyrin repeat proteins (WARPs) represent a highly dynamic and diverse part of the Wolbachia pangenome and remain thus far, largely uncharacterized. Here, we perform molecular and genetic screens to identify interactions between Wolbachia wMel WARPs and their target host proteins in Drosophila melanogaster. Our results identify strong interactions of two Wolbachia proteins, WARP434 and WARP754, with two host targets (CG11327 and Ptp61F, respectively). Heterologous expression of these two WARPs is extremely toxic in Drosophila tissues and the toxicity is dependent on the ankyrin repeat domain of each WARP. Importantly, knockdown of the host targets alleviates toxicity, confirming WARP/target interactions. Finally, antibodies targeting both WARPs show expression by Wolbachia during infection of Drosophila cells. Understanding how Wolbachia manipulates its host biology and which host pathways it targets during infection will help us divine how the most prevalent intracellular bacterial parasite on Earth interacts with its insect hosts at the molecular level. Our screen is the first step towards that goal. ImportanceMolecular interactions drive co-evolutionary arms races between hosts and pathogens. These interactions shape the structure and function of both host and parasite proteins, enabling immunity or virulence during infection. Understanding the molecular details that unfold during these events illustrates not only how hosts and parasites co-evolve at the molecular level but also may help characterize the function of poorly understood proteins. The most prevalent intracellular infection on earth is Wolbachia pipientis, with between 40-60% of insects harboring the bacterial symbiont. Understanding how Wolbachia infects host cells and the molecular tools it uses to alter cell biology is critical to the use of the microbe in vector control. Here, we identify Wolbachia proteins used by the symbiont to interface with specific host proteins. Understanding the molecular mechanisms underlying this host-microbe interaction will shed light on how an important symbiont, used in the control of vector populations and disease transmission, uses WARPs to interact with host targets and how targeting this host protein contributes to infection.

microbiology↗

bioRxiv2020

Regulation of Wolbachia proliferation by the amplification and deletion of an addictive genomic island

Wolbachia is one of the most prevalent bacterial endosymbionts, infecting approximately 40% of terrestrial arthropod species. Wolbachia is often a reproductive parasite but can also provide fitness benefits to its host, as, for example, protection against viral pathogens. This protective effect is currently being applied to fight arboviruses transmission by releasing Wolbachia-transinfected mosquitoes. Titre regulation is a crucial aspect of Wolbachia biology. Higher titres can lead to stronger phenotypes and fidelity of transmission but can have a higher cost to the host. Since Wolbachia is maternally transmitted, its fitness depends on host fitness, and, therefore, its cost to the host may be under selection. Understanding how Wolbachia titres are regulated and other aspects of Wolbachia biology has been hampered by the lack of genetic tools. Here we developed a forward genetic screen to identify new Wolbachia over-proliferative mutant variants. We characterized in detail two new mutants, wMelPop2 and wMelOctoless, and show that the amplification or loss of the Octomom genomic region lead to over-proliferation. These results confirm previous data and expand on the complex role of this genomic region in the control of Wolbachia proliferation. Both new mutants shorten the host lifespan and increase antiviral protection. Moreover, we show that Wolbachia proliferation rate in Drosophila melanogaster depends on the interaction between Octomom copy number, the host developmental stage, and temperature. Our analysis also suggests that the life shortening and antiviral protection phenotypes of Wolbachia are dependent on different, but related, properties of the endosymbiont; the rate of proliferation and the titres near the time of infection, respectively. Altogether, we demonstrate the feasibility of a novel and unbiased experimental approach to study Wolbachia biology, which can be further adapted to characterize other genetically intractable bacterial endosymbionts.

microbiology↗