Abstract

Detailed phenotypic characterization reveals that several BAK1 fusion proteins with C-terminal tags strongly impair complementation of bak1 null mutants with respect to responsiveness to the bacterial pathogen-associated molecular patterns flagellin and EF-Tu. This raises concerns about the widespread use of such protein variants of this important regulatory Leu-rich repeat receptor-like kinase (RLK) for functional analyses of RLK-based signaling.

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