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Botrytis cinerea  is an important plant pathogenic fungus with a wide range of host. It usually produces black-colored sclerotia (BS) due to deposition of 1,8-dihydroxynaphthalene melanin in sclerotial melanogenesis. Our previous study (Zhou et al.,  2018 ) reported six  B. cinerea  isolates producing orange-colored sclerotia (OS) with deficiency in sclerotial melanogenesis. Comparison of ecological fitness (conidia, mycelia, sclerotia), natural distribution, and melanogenesis of selected BS and OS isolates suggests that sclerotia play an important role in the disease cycle caused by  B. cinerea . However, the molecular mechanism for formation of the OS  B. cinerea  remains unknown. This study was done to unravel the molecular mechanism for the sclerotial melanogenesis deficiency in the OS isolates. We found that all the five sclerotial melanogenesis genes ( bcpks12, bcygh1, bcbrn1/2, bcscd1 ) were down-regulated in OS isolates, compared to the genes in the BS isolates. However, the sclerotial melanogenesis-regulatory gene  bcsmr1  had similar expression in both types of sclerotia, suggesting the sclerotial melanogenesis deficiency is due to loss-of-function of  bcsmr1 , rather than lack of expression of  bcsmr1 . Therefore, we cloned  bcsmr1  from OS ( bcsmr1   OS  ) and BS ( bcsmr1   BS  ) isolates, and found a single-nucleotide deletion in  bcsmr1   OS  . The single-nucleotide deletion caused formation of a premature stop codon in the open reading frame of  bcsmr1   OS  , resulting in production of a 465-aa truncated protein. The transcription activity of the truncated protein was greatly reduced, compared to that of the 935-aa full-length protein encoded by  bcsmr1   BS   in the BS isolates. The function of  bcsmr1   OS   was partially complemented by  bcsmr1   BS  . This study not only elucidated the molecular mechanism for formation of orange-colored sclerotia by the spontaneous mutant XN-1 of  B. cinerea , but also confirmed the regulatory function of  bcsmr1  in sclerotial melanogenesis of  B. cinerea .

A Single-Nucleotide Deletion in the Transcription Factor Gene bcsmr1 Causes Sclerotial-Melanogenesis Deficiency in Botrytis cinerea