Prioritizing MCDC test cases by spectral analysis of Boolean functions

Test case prioritization aims at scheduling test cases in an order that improves some performance goal. One performance goal is a measure of how quickly faults are detected. Such prioritization can be performed by exploiting the Fault Exposing Potential (FEP) parameters associated to the test cases. FEP is usually approximated by mutation analysis under certain fault assumptions. Although this technique is effective, it could be relatively expensive compared to the other prioritization techniques. This study proposes a cost-effective FEP approximation for prioritizing Modified Condition Decision Coverage (MCDC) test cases. A strict negative correlation between the FEP of a MCDC test case and the influence value of the associated input condition allows to order the test cases easily without the need of an extensive mutation analysis. The method is entirely based on mathematics and it provides useful insight into how spectral analysis of Boolean functions can benefit software testing

Additional file 3: Table S2. of BET bromodomain inhibitors and agonists of the beta-2 adrenergic receptor identified in screens for compounds that inhibit DUX4 expression in FSHD muscle cells

Collection of compounds that target epigenetic modifier proteins. (XLSX 33 kb

Increased DUX4 expression during muscle differentiation correlates with decreased SMCHD1 protein levels at D4Z4

<p>Facioscapulohumeral muscular dystrophy is caused by incomplete epigenetic repression of the transcription factor DUX4 in skeletal muscle. A copy of <i>DUX4</i> is located within each unit of the D4Z4 macrosatellite repeat array and its derepression in somatic cells is caused by either repeat array contraction (FSHD1) or by mutations in the chromatin repressor SMCHD1 (FSHD2). While DUX4 expression has thus far only been detected in FSHD muscle and muscle cell cultures, and increases with <i>in vitro</i> myogenic differentiation, the D4Z4 chromatin structure has only been studied in proliferating myoblasts or non-myogenic cells. We here show that SMCHD1 protein levels at D4Z4 decline during muscle cell differentiation and correlate with DUX4 derepression. In FSHD2, but not FSHD1, the loss of SMCHD1 repressor activity is partially compensated by increased Polycomb Repressive Complex 2 (PRC2)–mediated H3K27 trimethylation at D4Z4, a situation that can be mimicked by SMCHD1 knockdown in control myotubes. In contrast, moderate overexpression of SMCHD1 results in DUX4 silencing in FSHD1 and FSHD2 myotubes demonstrating that DUX4 derepression in FSHD is reversible. Together, we show that in FSHD1 and FSHD2 the decline in SMCHD1 protein levels during muscle cell differentiation renders skeletal muscle sensitive to DUX4.</p