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Technological developments have facilitated the application of genomics techniques at single-cell resolution.
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To properly characterise and investigate mosaic aneuploidy, it is therefore necessary to study individual cells rather than bulk populations. Similarly, mosaic aneuploidy is observed in populations of embryonic stem cells. Previous studies using array Comparative Genomic Hybridisation (aCGH) have shown that aneuploidies that arise during very early embryonic development are frequently mosaic in character, such that the copy number gain or loss only affects a fraction of the cells in the embryo these are referred to as mosaic aneuploidies. Aneuploidy-driven expression changes have been observed in yeast, Drosophila, and human cell lines at both the mRNA and the protein level. While the expression levels of genes on chromosomes with an aneuploidy are buffered in some cases, these mechanisms rarely fully compensate for the additional or missing gene copy and may only act on a gene-by-gene basis.
They occur commonly during early human development, cause some human disease (Edwards, Patau and Down syndromes), and are implicated in critical failures at the pre-implantation stage of development. However, detection of aneuploidies using conventional single-cell DNA-sequencing protocols is slow and expensive.īackground Aneuploidies are gains or losses of entire chromosomes. A cell that harbours an aneuploidy exhibits disrupted gene expression patterns which can alter its behaviour. Aneuploidies frequently affect only a subset of cells in a sample this is known as “mosaic” aneuploidy. They are seen commonly in cancer, embryonic stem cells, human embryos, and in various trisomic diseases.
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