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The Coding and Noncoding Architecture of the Genome


Caulobacter crescentus is a model system for studying asymmetric cell division, a fundamental process that, through differential gene expression in the two daughter cells, enables the generation of cells with different fates. To explore how the genome directs and maintains asymmetry upon cell division, we performed a coordinated analysis of multiple genomic and proteomic datasets to identify the RNA and protein coding features in the C. crescentus genome. Our integrated analysis identifies many new genetic regulatory elements, adding significant regulatory complexity to the C. crescentus genome. Surprisingly, 75.4% of protein coding genes lack a canonical translation initiation sequence motif (the Shine-Dalgarno site) which hybridizes to the 3′ end of the ribosomal RNA allowing translation initiation. We find Shine-Dalgarno sites primarily inside of genes where they cause translating ribosomes to pause, possibly allowing nascent proteins to correctly fold. With our detailed map of genomic transcription and translation elements, a systems view of the genetic network that controls asymmetric cell division is within reach.


Vyšlo v časopise: The Coding and Noncoding Architecture of the Genome. PLoS Genet 10(7): e32767. doi:10.1371/journal.pgen.1004463
Kategorie: Research Article
prolekare.web.journal.doi_sk: https://doi.org/10.1371/journal.pgen.1004463

Souhrn

Caulobacter crescentus is a model system for studying asymmetric cell division, a fundamental process that, through differential gene expression in the two daughter cells, enables the generation of cells with different fates. To explore how the genome directs and maintains asymmetry upon cell division, we performed a coordinated analysis of multiple genomic and proteomic datasets to identify the RNA and protein coding features in the C. crescentus genome. Our integrated analysis identifies many new genetic regulatory elements, adding significant regulatory complexity to the C. crescentus genome. Surprisingly, 75.4% of protein coding genes lack a canonical translation initiation sequence motif (the Shine-Dalgarno site) which hybridizes to the 3′ end of the ribosomal RNA allowing translation initiation. We find Shine-Dalgarno sites primarily inside of genes where they cause translating ribosomes to pause, possibly allowing nascent proteins to correctly fold. With our detailed map of genomic transcription and translation elements, a systems view of the genetic network that controls asymmetric cell division is within reach.


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