Shinde, M. | bioRxiv Science

bioRxiv2019

ChassiDex: A microbial database useful for synthetic biology applications

ChassiDex is an open-source, non-profit online host organism database that houses a repository of molecular, biological and genetic data for model organisms with applications in synthetic biology. The structured user-friendly environment makes it easy to browse information. The database consists of a page for each model organism subdivided into sections such as Growth Characteristics, Strain diversity, Culture sources, Maintenance protocol, Transformation protocol, BioBrick parts and commonly used vectors. With tools such as CUTE built for codon usage table generator, it is also easy to generate and download accurate novel codon tables for unconventional hosts in suitable formats. This database was built as a project for the International Genetically Engineered Machine Competition in 2017 with the mission of making it easy to shift from working with one host organism to another unconventional host organism for any researcher in the field of synthetic biology. The code along with other instructions for the usage of the database and tools are publicly available at the GitHub page. We encourage the synthetic biology community to contribute to the database by adding data for any additional or existing host organism.\n\nhttps://chassidex.org; https://github.com/ChassiDex

synthetic biology↗

bioRxiv2019

A role of cellular translation regulation associated with toxic Huntingtin protein

Huntingtons disease (HD) is a severe neurodegenerative disorder caused by poly Q repeat expansion in the Huntingtin (Htt) gene. While the Htt amyloid aggregates are known to affect many cellular processes, its role in translation is not addressed. Here we report pathogenic Htt expression causes protein synthesis deficit in cells. We find a functional prion-like protein, the translation regulator Orb2 to be sequestered by Htt aggregates. Coexpression of Orb2 can partially rescue the lethality associated with poly Q expanded Htt. These findings can be relevant for HD as human homologs of Orb2 also can be sequestered by pathogenic Htt aggregates. Our work suggests that translation dysfunction could be one of the contributors in the pathogenesis of HD and new therapies targeting protein synthesis pathways might help alleviate disease symptoms.

cell biology↗