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. 2021 May 6;10(5):563. doi: 10.3390/pathogens10050563

Figure 4.

Figure 4

Proposed model for the role of iGSLs upon an infection with Plasmodiophora brassicae in Brassica napus and interplay between iGSLs and aGSLs. (a) Resistant cultivars might maintain the water status in leaves by involving breakdown products of aGSLs in stomatal closure. Upregulation of aGSL contents was shown to be mediated by IAA5, IAA6 and IAA19. Stability of these auxin-responsive proteins might be prolonged by inhibition of the TIR1 receptor with conjugated I3M breakdown products. (b) Susceptible cultivars might be restrained in their production of I3M breakdown products due to low iGSL contents. This might lead to degradation of IAA5, IAA6 and IAA19 through IAA and subsequent drop in contents of aGSLs. (c) Inhibition of the TIR1 receptor by I3M breakdown products in resistant cultivars might maintain functional auxin response despite higher IAA contents during an infection. (d) Lower levels of iGSLs and subsequent lower levels of I3M breakdown products might lead to a positive feedback response caused by high auxin concentrations. Legend: IAA = indole-3-acetic acid; BP = breakdown products of glucobrassicin; TIR1 = transport inhibitor response 1, IAA receptor; AUX/IAA = auxin responsive proteins, mostly IAA repressive proteins; IAA5, 6, 19 = auxin responsive proteins, inhibit WRKY63; WRKY63 = transcription factor, represses expression of MYB28/29; MYB28/29 = transcription factors, positively regulate biosynthetic genes in the synthesis of aGSLs.