2024-03-29T02:18:47Zhttp://digital.csic.es/dspace-oai/requestoai:digital.csic.es:10261/1289402021-12-28T16:02:38Zcom_10261_128com_10261_1col_10261_381
Fernández-Álvarez, Alfonso
Elías-Villalobos, Alberto
Ibeas, José I.
2016-02-10T09:20:03Z
2016-02-10T09:20:03Z
2010
Plant Signaling and Behavior 5(4): 412-414 (2010)
1559-2316
http://hdl.handle.net/10261/128940
10.4161/psb.5.4.10805
1559-2324
http://dx.doi.org/10.13039/501100004837
http://dx.doi.org/10.13039/501100003339
http://dx.doi.org/10.13039/501100011011
20061799
Fungal plant pathogenesis involves complex crosstalk between fungi and their plant hosts. In the case of biotrophic fungi, the host interaction is finely controlled to maintain plant viability during infection since the fungus depends on the survival of colonized plant cells. Many proteins which participate in this process are thought to be glycosylated. Thus, defects in the glycosylation of fungal proteins might alter the normally attenuated plant response and consequently affect fungal progression. O-mannosyltransferases are responsible for adding mannose residues onto target proteins, with each O-mannosyltransferase having individual target specificities. In an earlier study, we showed that O-mannosylation is essential for Ustilago maydis virulence. We found that the loss of O-mannosyltransferase PMT4 was associated with a reduced formation frequency of the invasive morphogenic structure known as the appressorium, combined with a loss in their ability to penetrate plant cuticle. Here, we discuss the possible molecular causes of these phenotypes and present additional evidence, which argue against an alteration of plant response to fungal infection as the primary cause of the Δpmt4 phenotype.
eng
closedAccess
The requirement for protein O-mannosylation for Ustilago maydis virulence seems to be linked to intrinsic aspects of the infection process rather than an altered plant response
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