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Lr1-mediated leaf rust resistance pathways of transgenic wheat lines

ABSTRACT: The wheat gene Lr1 imparts resistance to certain races of the leaf rust pathogen Puccinia triticina. However, the biological basis underlying the complex resistance mechanisms remains largely unknown. Gene expression profiling analyses using the Affymetrix GeneChip® Wheat Genome Array were performed with six independent Lr1 transgenic lines sampled before inoculation (0h) and at 6 and 24 h after inoculation with the avirulent P. triticina race CCDS. For the 6 and 24 h time points, 3 384 probe sets corresponding to 2 978 transcripts were differentially expressed as compared to the plants before inoculation. Genes involved in defence signalling were triggered as early as 6 h post inoculation (HPI) and included COI1, the primary component of jasmonic acid signalling. By 24 HPI, a shift in plant cellular metabolism, namely carbon conservation, was notable. The enzymes of glycolysis and gluconeogenesis were down-regulated, however, enzymes linked to alternative carbon sequestration processes such as the glyoxylate cycle were up-regulated. Also at 24 HPI, various secondary signalling molecules belonging to the various hormone signalling pathways were triggered. These microarray data suggest that the Lr1 mediated leaf rust resistance is achieved by early onset of defence signalling followed by co-ordinated interplay of metabolism alteration and elicitation of defence responses. We used microarrays to detail the early gene expression events underlying Lr1-mediated resistance to Puccinia triticina pathogen in wheat.

ORGANISM(S): Triticum aestivum

PROVIDER: GSE32151 | GEO | 2012/09/14

SECONDARY ACCESSION(S): PRJNA147645

REPOSITORIES: GEO

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Project description:Wheat leaf rust caused by the pathogenic fungus Puccinia triticina, is a serious threat to bread wheat and durum production in many areas of the world. This plant-pathogen interaction has been studied extensively at the molecular genetics level, however proteomics data are still relatively scarce. The present study investigated temporal changes in the abundance of the apoplastic fluid proteome of wheat leaves infected with either virulent or avirulent races of P. triticina, using a label-free LC-MS-based approach. In general, there was very little difference between inoculated and control apoplastic proteomes as a result of either race of pathogen, until haustoria had become well established in the incompatible interaction, although the resistant host responds to pathogen challenge sooner than the susceptible. In the earlier samplings (up to 72 h after inoculation), there were 46 host proteins with significantly changing abundance, however pathogen proteins were detected only rarely and not reproducibly. This is consistent with the hemi-biotrophic life-style of P. triticina; the pathogen infection is characterized by an early phase of a symbiosis-like relationship, followed by a later stage of pathogenesis, with tissue damage and parasitism. The majority of the host proteins with altered abundance up to 72 h post-inoculation were pathogen-response-related, including peroxidases, chitinases, β-1-3-endo-glucanases and PR-proteins. Five days after inoculation with the incompatible race it was possible to detect 150 PT proteins and 117 host proteins which had significantly increased in abundance as well as 33 host proteins which had significantly decreased in abundance and which represent potential targets of pathogen effectors. The pathogen-expressed proteins – seen most abundantly in the incompatible interaction – were mostly uncharacterized proteins, however many of their functions could be inferred through homology-matching with pBLAST. Pathogen proteins also included several candidate effector proteins, some novel and some which have been reported previously from the purified haustoria proteome.

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Lr1-mediated leaf rust resistance pathways of transgenic wheat lines

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