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Biology subjects

Abad, L.

Publications and source records attributed to Abad, L..

3 recordsLinked to original sources

A novel stabilization mechanism accommodating genome length variation in evolutionarily related viral capsids

Tailed bacteriophages are one of the most numerous and diverse group of viruses. They store their genome at quasi-crystalline densities in capsids built from multiple copies of proteins adopting the HK97-fold. The high density of the genome exerts an internal pressure, requiring a maturation process that reinforces their capsids. However, it is unclear how capsid stabilization strategies have adapted to accommodate the evolution of larger genomes in this virus group. Here we characterized a novel capsid reinforcement mechanism in two evolutionary-related actinobacteriophages that modifies the length of a stabilization protein to accommodate a larger genome while maintaining the same capsid size. We used cryo-EM to reveal that capsids contained split hexamers of HK97-fold proteins with a stabilization protein in the chasm. The observation of split hexamers in mature capsids was unprecedented, so we rationalized this result mathematically, discovering that icosahedral capsids can be formed by all split or skewed hexamers as long as their T-number is not a multiple of three. Our results suggest that analogous stabilization mechanisms can be present in other icosahedral capsids, and they provide a strategy for engineering capsids accommodating larger DNA cargoes as gene delivery systems. Significance StatementHow capsids are stabilized and change size is an important part of understanding how to design protein containers and understand viral evolution. We describe a novel capsid stability mechanism that allows the capsid to package a larger genome without changing the capsid architecture and have predicted other capsids using this mechanism. Beyond the evolutionary implications, our findings provide a mechanism to increase the amount of DNA packaged in a capsid, offering a solution to engineer gene delivery systems with larger DNA content, a pressing challenge in gene therapy.

molecular biology↗

Analysis of in-patient evolution of Escherichia coli reveals potential links to relapse of bone and joint infections

Bone and joint infections (BJIs) are difficult to treat and affect a growing number of patients, in which relapses are observed in 10-20% of the case. These relapses, which call for prolonged antibiotic treatment and increase the risk of emergence of resistance, may originate from ill understood adaptation of the pathogen to the host. Here, we studied three pairs of Escherichia coli strains corresponding to three cases of BJIs and their relapse to better understand in-patient adaptation. Whole genome comparison presented evidence for positive selection with prevalence of non-synonymous and loss of function mutations. Phenotypic characterization showed that biofilm formation capacity was not modified, contrary to what is usually described in such relapse cases. Although virulence was not modified, we identified the loss of two virulence factors (namely an AFA afimbrial adhesin and a YadA-like adhesin) contributing to immune system evasion in one of the studied relapse strain. Other selected strategies likely helped the relapse strains to outcompete competitors through global growth optimization and colicin production. This work highlights the variety of strategies allowing in-patient adaptation in BJIs.

microbiology↗

Mycobacterium trehalose polyphleates are required for mycobacteriophage infection

Mycobacteriophages are good model systems for understanding their bacterial hosts and show promise as therapeutic agents for nontuberculous mycobacterium infections. However, little is known about phage recognition of Mycobacterium cell surfaces, or mechanisms of phage resistance. We show here that surface-exposed trehalose polyphleates (TPPs) are required for infection of Mycobacterium abscessus and Mycobacterium smegmatis by clinically useful phages BPs and Muddy, and that TPP loss leads to defects in adsorption, infection, and confers resistance. Transposon mutagenesis indicates that TPP loss is the primary mechanism for phage resistance. Spontaneous phage resistance occurs through TPP loss, and some M. abscessus clinical isolates are phage-insensitive due to TPP absence. Both BPs and Muddy become TPP-independent through single amino acid substitutions in their tail spike proteins, and M. abscessus mutants resistant to TPP-independent phages reveal additional resistance mechanisms. Clinical use of BPs and Muddy TPP-independent mutants should preempt phage resistance caused by TPP loss.

microbiology↗