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Characterization and Identification of a woody lesion mimic mutant lmd, showing defence response and resistance to Alternaria alternate in birch

Lesion mimic mutants (LMM) usually show spontaneous cell death and enhanced defence responses similar to hypersensitive response (HR) in plants. Many LMM have been reported in rice, wheat, maize, barley, Arabidopsis, etc., but little was reported in xylophyta. BpGH3.5 is an early auxin-response fact...

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Detalles Bibliográficos
Autores principales: Li, Ranhong, Chen, Su, Liu, Guifeng, Han, Rui, Jiang, Jing
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5595973/
https://www.ncbi.nlm.nih.gov/pubmed/28900274
http://dx.doi.org/10.1038/s41598-017-11748-2
Descripción
Sumario:Lesion mimic mutants (LMM) usually show spontaneous cell death and enhanced defence responses similar to hypersensitive response (HR) in plants. Many LMM have been reported in rice, wheat, maize, barley, Arabidopsis, etc., but little was reported in xylophyta. BpGH3.5 is an early auxin-response factor which regulates root elongation in birch. Here, we found a T-DNA insertion mutant in a BpGH3.5 transgenic line named lmd showing typical LMM characters and early leaf senescence in Betula platyphylla × B. pendula. lmd showed H(2)O(2) accumulation, increased SA level and enhanced resistance to Alternaria alternate, compared with oe21 (another BpGH3.5 transgenic line) and NT (non-transgenic line). Cellular structure observation showed that programmed cell death occurred in lmd leaves. Stereomicroscope observation and Evans’ blue staining indicated that lmd is a member of initiation class of LMM. Transcriptome analysis indicated that defence response-related pathways were enriched. Southern-blot indicated that there were two insertion sites in lmd genome. Genome re-sequencing and thermal asymmetric interlaced PCR (TAIL-PCR) confirmed the two insertion sites, one of which is a T-DNA insertion in the promoter of BpEIL1 that may account for the lesion mimic phenotype. This study will benefit future research on programmed cell death, HR and disease resistance in woody plants.