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Trisomy, a form of aneuploidy wherein the cell possesses an additional copyof a specific chromosome, exhibits a high correlation with cancer. Studies fromacross different hosts, cell-lines, and labs into the cellular effects inducedby aneuploidy have conflicted, ranging from small, chaotic global changes tolarge instances of either overexpression or underexpression throughout thetrisomic chromosome. We ascertained that conflicting findings may be correctbut miss the overarching ground truth due to careless use of thresholds. Tocorrect this deficiency, we introduce the Meta-analytic Operation ofThreshold-independent Filtering (MOTiF) method, which begins by providing apanoramic view of all thresholds, transforms the data to eliminate the effectsaccounted for by known mechanisms, and then reconstructs an explanation of themechanisms that underly the difference between the baseline and theuncharacterized effects observed. As a proof of concept, we applied MOTiF tohuman colonic epithelial cells, discovering a uniform decrease in geneexpression levels throughout the genome, which while significant, is beneathmost common thresholds. Using Hi-C data we identified the structural correlate,wherein the physical genomic architecture condenses, compactifying in auniform, genome-wide manner, which we hypothesize is a robustness mechanismcounteracting the addition of a chromosome. We were able to decompose the geneexpression alterations into three overlapping mechanisms: the raw chromosomecontent, the genomic compartmentalization, and the global structuralcondensation. While further studies must be conducted to corroborate thehypothesized robustness mechanism, MOTiF presents a useful meta-analytic toolin the realm of gene expression and beyond.

Meta-Analytic Operation of Threshold-independent Filtering (MOTiF) Reveals Sub-threshold Genomic Robustness in Trisomy