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BMC Genomics

, 18:305

Human and rodent genomics


BackgroundThe quantitative relations between RNA and protein are fundamental to biology and are still not fully understood. Across taxa, it was demonstrated that the protein-to-mRNA ratio in steady state varies in a direction that lessens the change in protein levels as a result of changes in the transcript abundance. Evidence for this behavior in tissues is sparse. We tested this phenomenon in new data that we produced for the mouse auditory system, and in previously published tissue datasets. A joint analysis of the transcriptome and proteome was performed across four datasets: inner-ear mouse tissues, mouse organ tissues, lymphoblastoid primate samples and human cancer cell lines.

ResultsWe show that the protein levels are more conserved than the mRNA levels in all datasets, and that changes in transcription are associated with translational changes that exert opposite effects on the final protein level, in all tissues except cancer. Finally, we observe that some functions are enriched in the inner ear on the mRNA level but not in protein.

ConclusionsWe suggest that partial buffering between transcription and translation ensures that proteins can be made rapidly in response to a stimulus. Accounting for the buffering can improve the prediction of protein levels from mRNA levels.

KeywordsInner ear Cochlea Mass spectrometry RNA-seq Translation AbbreviationsRFCBRelaxed FC Based

RMSERoot mean square error

WAPWeighted average protein

WAPTRWeighted average protein-transcript ratio

DEDifferentially expressed

FCFold change

FDRFalse discovery rate

GOGene ontology

LCLLymphoblastoid cell line

MAMajor axis

MDSMulti-dimensional scaling

MMTMultiple mouse tissues

mRNAmessenger RNA

MSMass spectrometry

OLSOrdinary least square

P0Post-natal day 0

PTRProtein-transcript ratio

RPKMReads per kilobase per million

SILACStable isotope labeling with amino acids in cell culture

Electronic supplementary materialThe online version of this article doi:10.1186-s12864-017-3683-9 contains supplementary material, which is available to authorized users.



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