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De novo emergence, existence, and demise of a protein-coding gene in murids [chinese hamster]

ABSTRACT: De novo emergence, existence, and demise of a protein-coding gene in murids [chinese hamster]

PROVIDER: PRJNA882483 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21643385_1.fastq.gz	Fastqsanger.gz
	SRR21643385_2.fastq.gz	Fastqsanger.gz
	SRR21643386_1.fastq.gz	Fastqsanger.gz
	SRR21643386_2.fastq.gz	Fastqsanger.gz

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De novo emergence, existence, and demise of a protein-coding gene in murids [chinese hamster]

Project description:Genes, principal units of genetic information, vary in complexity and evolutionary history. Less-complex genes (e.g. long non-coding RNA (lncRNA) expressing genes), readily emerge de novo from non-genic sequences and have high evolutionary turnover. Genesis of a gene is facilitated by adoption of functional genic sequences from retrotransposon insertions. However, protein-coding sequences in extant genomes rarely lack any connection to an ancestral protein-coding sequence. Here, we describe remarkable evolution of the murine gene D6Ertd527e and its orthologs in the rodent Muroidea superfamily. The D6Ertd527e emerged in a common ancestor of mice and hamsters as an lncRNA-expressing gene. A major contributing factor was a long terminal repeat (LTR) retrotransposon insertion carrying an oocyte-specific promoter and one of the first exons of the gene. The gene survived as an oocyte-specific lncRNA in several extant rodents while in some others the gene or its expression was lost. In the ancestral lineage of Mus musculus, the gene acquired protein-coding capacity where the bulk of the coding sequence formed through CAG (AGC) trinucleotide repeat expansion and duplications. These events gave rise to a cytoplasmic serine-rich maternal protein, which has no discernable role. Knock-out of D6Ertd527e in mice affects neither fertility nor the maternal transcriptome. While this evolving gene is not showing a notable function in laboratory mice, its documented evolutionary history in Muroidea during the last ~40 million years provides a textbook example of how a several common mutation events can support de novo gene formation, evolution of protein-coding capacity, as well as gene’s demise.

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De novo emergence, existence, and demise of a protein-coding gene in murids

Project description:De novo emergence, existence, and demise of a protein-coding gene in murids

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De novo emergence, existence, and demise of a protein-coding gene in murids [mouse]

Project description:De novo emergence, existence, and demise of a protein-coding gene in murids [mouse]

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De novo emergence, existence, and demise of a protein-coding gene in murids

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Project description:Gene expression is a key determinant of phenotypes that made Chinese Hamster Ovary (CHO) cells, with their human-like glycosylation profile and high protein titers, one of the most widely used cells for the production of therapeutic proteins and biopharmaceuticals. Engineering CHO gene expression thus holds a key to improve drug quality and cost effective production. However, the success of engineering gene expression or ectopic activation of silent genes to optimize desired pathways requires accurate annotation of the underlying regulatory elements and the transcription start site (TSS). Unfortunately, to date, most TSSs of CHO-expressed genes and the ~50% of hamster genes that are silent in CHO were computationally predicted and are frequently inaccurate. To oust this hurdle, we report revised TSSs annotations for 15,308 Chinese Hamster genes and 4,145 non-coding RNAs based on experimental data from CHO K1 cells and 10 hamster tissues. In the example of the glycosyltransferase gene Mgat3, we further demonstrate how accurate annotations readily facilitate activating silent genes by CRISPRa. Together, we envision that our annotation and data from the Chinese Hamster will provide a rich resource for the CHO community, improve genome engineering efforts and additionally aid comparative and evolutionary studies.

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