Botrytis cinerea is the causal agent of gray mold diseases in a range of dicotyledonous plant species. The fungus can reproduce asexually by forming macroconidia for dispersal and sclerotia for survival; the latter also participate in sexual reproduction by bearing the apothecia after fertilization by microconidia. Light induces the differentiation of conidia and apothecia, while sclerotia are exclusively formed in the absence of light. The relevance of light for virulence of the fungus is not obvious; infections are observed under natural illumination as well as in constant darkness. By a random mutagenesis approach, we identified a novel virulence-related gene encoding a GATA transcription factor (BcLTF1 for light-responsive TF1) with characterized homologues in Aspergillus nidulans (NsdD) and Neurospora crassa (SUB-1). By deletion and overexpression of bcltf1, we confirmed the predicted role of the TF in virulence, and discovered furthermore its functions in regulation of light-dependent differentiation, the equilibrium between production and scavenging of reactive oxygen species (ROS), and secondary metabolism. Microarray analyses revealed 293 lightresponsive genes in B. cinerea B05.10 including five further TF-encoding genes (BcLTF2-6), and that the expression levels of the majority of these genes (66%) are modulated by BcLTF1. Bcltf2 encodes a C2H2-TF which is the homologue of N. crassa SAH-1 (short-aerial-hyphae-1). Expression levels are increased in mutants exhibiting a hyper-conidiation phenotype such as deletion mutants of BcLTF1, the VELVET protein BcVEL1 and the WHITE COLLAR-like TF BcWCL1, suggesting a role of BcLTF2 in regulation of conidiation. Indeed, Δbcltf2 mutants do not produce conidia in axenic culture and in planta. Notably, mutants form sclerotia under all illumination conditions indicating that the suppression of sclerotial development by light is likely due to the induction of conidiation rather than due to a direct suppression of the sclerotium differentiation program.