Garcia, L. E. | Search bioRxiv

bioRxiv2019

Gene expression is associated with virulence in murine macrophages infected with Leptospira spp

Leptospira genus contains species that affect human health with varying degrees of pathogenicity. In this context, we aimed to evaluate the differences in modulation of host gene expression by strains of Leptospira with varied virulence degrees. Our data showed a high number of differentilly expressed transcripts in murine macrophages following 6h of infection with both virulent and culture-attenuated L. interrogans and to a lesser degree, with the saprophyte strain L. biflexa. That suggests that certain genes are modulated by Leptospira infection independent of their degree of virulence, whether others are virulence and species associated. Pathway analysis indicated that Apoptosis, ATM Signaling and Cell Cycle: G2/M DNA Damage Checkpoint Regulation were exclusively regulated following infection with the virulent strain. Results demonstrated that species and virulence play a role during host response to Leptosppira spp in murine macrophages.\n\nAuthor summaryLeptospirosis is an infectious disease that is transmitted from animals to humans. It is a re-emerging neglected zoonosis that is found in a range of environments worldwide, most notably tropical regions prone to flooding. This bacteria is found in soil and water and are eliminated in the urine by rats, their natural host reservoir. Through skin contacts with the bacteria people or animals can get infected however the infection process is still poorly understood, such as the fact that different strains can cause different severity of illness. In this study, we aimed to evaluate the differences in modulation of host gene expression by strains of Leptospira varying in virulence. After transcriptomic analysis, the results showed a high number of differentially expressed genes after 6h of infection by virulent and attenuated L. interrogans, and to a lesser extent with L. biflexa saprophytic lineage. This suggests that RNAs are modulated after infection by Leptospira in macrophages, in a species and virulence related manner. It is hoped that the data produced will contribute to further our understanding on the pathogenesis of leptospirosis.

molecular biology↗

bioRxiv2018

Elucidating genomic patterns and recombination events in plant cybrid mitochondria

The maintenance of a dynamic equilibrium between the mitochondrial and nuclear genomes requires continuous communication and a high level of compatibility between them, so that alterations in one genetic compartment need adjustments in the other. The co-evolution of nuclear and mitochondrial genomes has been poorly studied, even though the consequences and effects of this interaction are highly relevant for human health, as well as for crop improvement programs and for genetic engineering. The mitochondria of plants represent an excellent system to understand the mechanisms of genomic rearrangements, chimeric gene formation, incompatibility between nucleus and cytoplasm, and horizontal gene transfer. We carried out detailed analyses of the mitochondrial genome (mtDNA) of a repeated cybrid between the solanaceae Nicotiana tabacum and Hyoscyamus niger. The mtDNA of the cybrid was intermediate between the size of parental mtDNAs and the sum of them. Noticeably, most of the homologous sequences inherited from both parents were lost. In contrast, the majority of the sequences exclusive of a single parent were maintained. The mitochondrial gene content included a majority of N. tabacum derived genes, but also chimeric, two-parent derived, and H. niger-derived genes in a tobacco nuclear background. Any of these alterations in the gene content could be the cause of CMS in the cybrid. The parental mtDNAs interacted through 28 homologous recombination events and a single case of illegitimate recombination. Three main homologous recombination mechanisms were recognized in the cybrid mitochondria. Break induced replication (BIR) pathway was the most frequent. We propose that BIR could be one of the mechanisms responsible for the loss of the majority of the repeated regions derived from H. niger.

molecular biology↗