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Lateral acquisition of genes is affected by the friendliness of their products.

ABSTRACT: A major factor in the evolution of microbial genomes is the lateral acquisition of genes that evolved under the functional constraints of other species. Integration of foreign genes into a genome that has different components and circuits poses an evolutionary challenge. Moreover, genes belonging to complex modules in the pretransfer species are unlikely to maintain their functionality when transferred alone to new species. Thus, it is widely accepted that lateral gene transfer favors proteins with only a few protein-protein interactions. The propensity of proteins to participate in protein-protein interactions can be assessed using computational methods that identify putative interaction sites on the protein. Here we report that laterally acquired proteins contain significantly more putative interaction sites than native proteins. Thus, genes encoding proteins with multiple protein-protein interactions may in fact be more prone to transfer than genes with fewer interactions. We suggest that these proteins have a greater chance of forming new interactions in new species, thus integrating into existing modules. These results reveal basic principles for the incorporation of novel genes into existing systems.

SUBMITTER: Gophna U

PROVIDER: S-EPMC3017175 | biostudies-literature | 2011 Jan

REPOSITORIES: biostudies-literature

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Lateral acquisition of genes is affected by the friendliness of their products.

Gophna Uri U Ofran Yanay Y

Proceedings of the National Academy of Sciences of the United States of America 20101213 1

A major factor in the evolution of microbial genomes is the lateral acquisition of genes that evolved under the functional constraints of other species. Integration of foreign genes into a genome that has different components and circuits poses an evolutionary challenge. Moreover, genes belonging to complex modules in the pretransfer species are unlikely to maintain their functionality when transferred alone to new species. Thus, it is widely accepted that lateral gene transfer favors proteins w ...[more]

PMID: 21149709

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Project description:Rationale: The anatomical substrate of skeletal muscle autonomic innervation has remained underappreciated since it was described many decades ago. As such, the structural and functional features of muscle sympathetic innervation are largely undetermined in both physiology and pathology, mainly due to methodological limitations in the histopathological analysis of small neuronal fibers in tissue samples. Amyotrophic lateral sclerosis (ALS) is a fatal neuromuscular disease which mainly targets motor neurons, and despite autonomic symptoms occurring in a significant fraction of patients, peripheral sympathetic neurons (SNs) are generally considered unaffected and, as such, poorly studied. Purpose: In this research, we compared sympathetic innervation of normal and ALS muscles, through structural analysis of the sympathetic network in human and murine tissue samples. Methods and Results: We first refined tissue processing to circumvent methodological limitations interfering with the detection of muscle sympathetic innervation. The optimized "Neuro Detection Protocol" (NDP) was validated in human muscle biopsies, demonstrating that SNs innervate, at high density, both blood vessels and skeletal myofibers, independent of the fiber metabolic type. Subsequently, NDP was exploited to analyze sympathetic innervation in muscles of SOD1G93A mice, a preclinical ALS model. Our data show that ALS murine muscles display SN denervation, which has already initiated at the early disease stage and worsened during aging. SN degeneration was also observed in muscles of MLC/SOD1G93A mice, with muscle specific expression of the SOD1G93A mutant gene. Notably, similar alterations in SNs were observed in muscle biopsies from an ALS patient, carrying the SOD1G93A mutation. Conclusion: We set up a protocol for the analysis of murine and, more importantly, human muscle sympathetic innervation. Our results indicate that SNs are additional cell types compromised in ALS and suggest that dysfunctional SOD1G93A muscles affect their sympathetic innervation.

Dataset Information

Lateral acquisition of genes is affected by the friendliness of their products.

Publications

Lateral acquisition of genes is affected by the friendliness of their products.

Similar Datasets

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