Literature DB >> 28382431

Regulation of conidiation in Botrytis cinerea involves the light-responsive transcriptional regulators BcLTF3 and BcREG1.

Beate Brandhoff1, Adeline Simon2, Anne Dornieden1, Julia Schumacher3.   

Abstract

Botrytis cinerea is a plant pathogenic fungus with a broad host range. Due to its rapid growth and reproduction by asexual spores (conidia), which increases the inoculum pressure, the fungus is a serious problem in different fields of agriculture. The formation of the conidia is promoted by light, whereas the formation of sclerotia as survival structures occurs in its absence. Based on this observation, putative transcription factors (TFs) whose expression is induced upon light exposure have been considered as candidates for activating conidiation and/or repressing sclerotial development. Previous studies reported on the identification of six light-responsive TFs (LTFs), and two of them have been confirmed as crucial developmental regulators: BcLTF2 is the positive regulator of conidiation, whose expression is negatively regulated by BcLTF1. Here, the functional characterization of the four remaining LTFs is reported. BcLTF3 has a dual function, as it represses conidiophore development by repressing bcltf2 in light and darkness, and is moreover essential for conidiogenesis. In bcltf3 deletion mutants conidium initials grow out to hyphae, which develop secondary conidiophores. In contrast, no obvious functions could be assigned to BcLTF4, BcLTF5 and BcLTF6 in these experiments. BcREG1, previously reported to be required for virulence and conidiogenesis, has been re-identified as light-responsive transcriptional regulator. Studies with bcreg1 overexpression strains indicated that BcREG1 differentially affects conidiation by acting as a repressor of BcLTF2-induced conidiation in the light and as an activator of a BcLTF2-independent conidiation program in the dark.

Entities:  

Keywords:  Botrytis cinerea; Conidiation; Conidiogenesis; Light; Transcription factor

Mesh:

Substances:

Year:  2017        PMID: 28382431     DOI: 10.1007/s00294-017-0692-9

Source DB:  PubMed          Journal:  Curr Genet        ISSN: 0172-8083            Impact factor:   3.886


  59 in total

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