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The human placenta exhibits a unique transcriptomic void

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Aye, Irving 
Avellino, Giulia 
Cook, Emma 
Lawson, Andrew RJ 


We have recently demonstrated that the human placenta exhibits a unique genomic architecture with an unexpectedly high mutation burden1 and it is also well recognized that the placenta uniquely expresses many genes2. However, the placenta is relatively understudied in systematic comparisons of gene expression in different organs. The aim of the present study was to identify transcripts which were uniquely absent or depleted, comparing the placenta with 46 other human organs or tissues. Here we show that 40/46 of the other organs had no transcripts which were selectively depleted and that of the remaining six, the liver had the largest number with 26. In contrast, the term placenta had 762 depleted transcripts. Gene Ontology analysis of this depleted set highlighted multiple pathways reflecting known unique elements of placental physiology. For example, transcripts associated with neuronal function are in the depleted set and this is expected given the lack of placental innervation3. However, analysis of the depleted transcripts in term samples demonstrated massive over representation of genes involved in mitochondrial function (P=5.8x10-10), including PGC-1α - the master regulator of mitochondrial biogenesis, and genes involved in polyamine metabolism (P=2.1x10-4). We conclude that the term placenta exhibits a unique metabolic environment.



CP: Developmental biology, CP: Molecular biology, Humans, Pregnancy, Female, Placenta, Transcriptome, Gene Expression Profiling, Mitochondria

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Cell Reports

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Medical Research Council (G1100221)
Medical Research Council (MR/K021133/1)
Cambridge University Hospitals NHS Foundation Trust (CUH) (146281)
Medical Research Council (G1100221/1)
This work was supported by the Medical Research Council (United Kingdom; G1100221 and MR/K021133/1) and the National Institute for Health Research (NIHR) Cambridge Biomedical Research Centre (Women’s Health theme). I.A. was funded by the Centre for Trophoblast Research (CTR) Next Generation Fellowship. G.A. is funded by the CTR PhD scholarship. A.R.J.L. and L.M.R.H. are funded by Wellcome PhD studentships
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