In the phytopathogenic basidiomycete Ustilago maydis, sexual and pathogenic development are tightly connected and controlled by the heterodimeric bE/bW transcription factor complex encoded by the b-mating type locus. The formation of the active bE/bW heterodimer leads to the formation of filaments, induces a G2 cell cycle arrest, and triggers pathogenicity. Here, we identify a set of 345 bE/bW responsive genes which show altered expression during these developmental changes; several of these genes are associated with cell cycle coordination, morphogenesis and pathogenicity. 90% of the genes that show altered expression upon bE/bW-activation require the zinc finger transcription factor Rbf1, one of the few factors directly regulated by the bE/bW heterodimer. Rbf1 is a novel master regulator in a multilayered network of transcription factors that facilitates the complex regulatory traits of sexual and pathogenic development.

Abstract-Mutation testing measures the adequacy of a test suite by seeding artificial defects (mutations) into a program. If a test suite fails to detect a mutation, it may also fail to detect real defects-and hence should be improved. However, there also are mutations which keep the program semantics unchanged and thus cannot be detected by any test suite. Such equivalent mutants must be weeded out manually, which is a tedious task. In this paper, we examine whether changes in coverage can be used to detect non-equivalent mutants: If a mutant changes the coverage of a run, it is more likely to be non-equivalent. In a sample of 140 manually classified mutations of seven Java programs with 5,000 to 100,000 lines of code, we found that: (a) the problem is serious and widespread-about 45% of all undetected mutants turned out to be equivalent; (b) manual classification takes time-about 15 minutes per mutation; (c) coverage is a simple, efficient, and effective means to identify equivalent mutants-with a classification precision of 75% and a recall of 56%; and (d) coverage as an equivalence detector is superior to the state of the art, in particular violations of dynamic invariants. Our detectors have been released as part of the open source JAVALANCHE framework; the data set is publicly available for replication and extension of experiments.

Mutation testing measures the adequacy of a test suite by seeding artificial defects (mutations) into a program. If a mutation is not detected by the test suite, this usually means that the test suite is not adequate. However, it may also be that the mutant keeps the program's semantics unchangedand thus cannot be detected by any test. Such equivalent mutants have to be eliminated manually, which is tedious.We assess the impact of mutations by checking dynamic invariants. In an evaluation of our JAVALANCHE framework on seven industrial-size programs, we found that mutations that violate invariants are significantly more likely to be detectable by a test suite. As a consequence, mutations with impact on invariants should be focused upon when improving test suites. With less than 3% of equivalent mutants, our approach provides an efficient, precise, and fully automatic measure of the adequacy of a test suite.

SUMMARYMutation testing measures the adequacy of a test suite by seeding artificial defects (mutations) into a program. If a test suite fails to detect a mutation, it may also fail to detect real defects—and hence should be improved. However, there are also mutations that keep the program semantics unchanged and thus cannot be detected by any test suite. Such equivalent mutants must be weeded out manually, which is a tedious task. In this paper, we examine whether changes in coverage can be used to detect non‐equivalent mutants: If a mutant changes the coverage of a run, it is more likely to be non‐equivalent. In a sample of 140 manually classified mutations of seven Java programs with 5000 to 100 000 lines of code, we found that (i) the problem is serious and widespread—about 45% of all undetected mutants turned out to be equivalent; (ii) manual classification takes time—about 15 min per mutation; (iii) coverage is a simple, efficient and effective means to identify equivalent mutants—with a classification precision of 75% and a recall of 56%; and (iv) coverage as an equivalence detector is superior to the state of the art, in particular violations of dynamic invariants. Our detectors have been released as part of the open‐source JAVALANCHE framework; the data set is publicly available for replication and extension of experiments. Copyright © 2012 John Wiley & Sons, Ltd.

Regulation of the cell cycle and morphogenetic switching during pathogenic and sexual development in Ustilago maydis is orchestrated by a concerted action of the a and b mating-type loci. Activation of either mating-type locus triggers the G2 cell cycle arrest that is a prerequisite for the formation of the infectious dikaryon; this cell cycle arrest is released only after penetration of the host plant. Here, we show that bW, one of the two homeodomain transcription factors encoded by the b mating-type locus, and the zinc-finger transcription factor Rbf1, a master regulator for pathogenic development, interact with Clp1 (clampless 1), a protein required for the distribution of nuclei during cell division of the dikaryon. In addition, we identify Cib1, a previously undiscovered bZIP transcription factor required for pathogenic development, as a Clp1-interacting protein. Clp1 interaction with bW blocks b-dependent functions, such as the b-dependent G2 cell cycle arrest and dimorphic switching. The interaction of Clp1 with Rbf1 results in the repression of the a-dependent pheromone pathway, conjugation tube formation, and the a-induced G2 cell cycle arrest. The concerted interaction of Clp1 with Rbf1 and bW coordinates a-and b-dependent cell cycle control and ensures cell cycle release and progression at the onset of biotrophic development.