Abstract
Phytophthora nicotianae is a devastating oomycete plant pathogen with a wide host range. On tobacco, it causes black shank, a disease that can result in severe economic losses. Deployment of host resistance is one of the most effective means of controlling tobacco black shank, but adaptation to complete and partial resistance by P. nicotianae can limit the long-term effectiveness of the resistance. The molecular basis of adaptation to partial resistance is largely unknown. RNAseq was performed on two isolates of P. nicotianae (adapted to either the susceptible tobacco genotype Hicks or the partially resistant genotype K 326 Wz/Wz) to identify differentially expressed genes (DEGs) during their pathogenic interactions with K 326 Wz/Wz and Hicks. Approximately 69% of the up-regulated DEGs were associated with pathogenicity in the K 326 Wz/Wz-adapted isolate when sampled following infection of its adapted host K 326 Wz/Wz. Thirty-one percent of the up-regulated DEGs were associated with pathogenicity in the Hicks-adapted isolate on K 326 Wz/Wz. A broad spectrum of over-represented gene ontology (GO) terms were assigned to down-regulated genes in the Hicks-adapted isolate. In the host, a series of GO terms involved in nuclear biosynthesis processes were assigned to the down-regulated genes in K 326 Wz/Wz inoculated with K 326 Wz/Wz-adapted isolate. This study enhances our understanding of the molecular mechanisms of P. nicotianae adaptation to partial resistance in tobacco by elucidating how the pathogen recruits pathogenicity-associated genes that impact host biological activities.
Highlights
Plant diseases are estimated to cause crop losses of 13% annually, imposing a major constraint on global crop production [1]
Root tissue colonized by P. nicotianae was obtained for RNA sequencing (RNAseq) by inoculating and harvesting the roots of seedlings 48 h post inoculation
At 48 hpi, slight browning of the roots was present and abundant sporangia were present around roots
Summary
Plant diseases are estimated to cause crop losses of 13% annually, imposing a major constraint on global crop production [1]. Deployment of complete and partial resistance in host plants is one of the most effective means of managing plant diseases and is an integral part of sustainable disease management that reduces the use of fungicides and other management inputs [2]. Wide distribution of cultivars with complete resistance places strong selection pressure on pathogen populations to overcome that resistance [3]. Various mechanisms utilized by plant pathogens to overcome complete resistance have been recognized, including loss of avirulence (Avr) gene products that trigger plant immunity, transposon insertions or mutations to the Avr gene sequence, acquisition of additional epistatic effectors that suppress the plant immune system without disrupting the original Avr gene [7], and endogenous small RNAs silencing Avr genes [8]. Despite our rapid improvement in understanding the molecular basis underlying complete resistance and how pathogens overcome it, mechanisms of plant pathogen adaptation to partial resistance remains largely unknown
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