H3K4/K9 acetylation and Lr28-mediated expression of six leaf rust responsive genes in wheat (Triticum aestivum)
Development of leaf rust-resistant cultivars is a priority during wheat breeding, since leaf rust causes major losses in yield. Resistance against leaf rust due to Lr genes is partly controlled by epigenetic modifications including histone acetylation that is known to respond to biotic/abiotic stres...
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Veröffentlicht in: | Molecular genetics and genomics : MGG 2019-02, Vol.294 (1), p.227-241 |
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Sprache: | eng |
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Zusammenfassung: | Development of leaf rust-resistant cultivars is a priority during wheat breeding, since leaf rust causes major losses in yield. Resistance against leaf rust due to
Lr
genes is partly controlled by epigenetic modifications including histone acetylation that is known to respond to biotic/abiotic stresses. In the present study, enrichment of H3K4ac and H3K9ac in promoters of six defense responsive genes (
N-acetyltransferase, WRKY 40, WRKY 70, ASR1, Peroxidase 12
and
Sarcosine oxidase
) was compared with their expression in a pair of near-isogenic lines (NILs) for the gene
Lr28
following inoculation with leaf rust pathotype ’77-5’; ChIP-qPCR was used for this purpose. The proximal and distal promoters of these genes contained a number of motifs that are known to respond to biotic stresses. The enrichment of two acetylation marks changed with passage of time; changes in expression of two of the six genes (
N-acetyltransferase
and
peroxidase12
), largely matched with changes in H3K4/H3K9 acetylation patterns of the two promoter regions. For example, enrichment of both the marks matched with higher expression of
N-acetyltransferase
gene in susceptible NIL and the deacetylation (H3K4ac) largely matched with reduced gene expression in resistant NIL. In
peroxidase12
, enrichment of H3K4ac and H3K9ac largely matched with higher expression in both the NILs. In the remaining four genes, changes in H3 acetylation did not always match with gene expression levels. This indicated complexity in the regulation of the expression of these remaining four genes, which may be controlled by other epigenetic/genetic regulatory mechanisms that need further analysis. |
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ISSN: | 1617-4615 1617-4623 |
DOI: | 10.1007/s00438-018-1500-z |