Nicotiana tabacumTTG1 contributes to ParA1-induced signalling and cell death in leaf trichomes

Abstract

suggesting the importance of H 2 O 2 in the pathway of HCD signal transduction from the trichomes to mesophylls. This pathway was no longer activated when leaf trichomes were treated with C51S, a ParA1 mutant protein defective in its interaction with N. tabacum TTG1 (NtTTG1), which is a trichome protein that binds ParA1, rather than C51S, in vitro and in trichome cells. The ParA1-NtTTG1 interaction and the HCD pathway were also abrogated when NtTTG1 was silenced in the trichomes. These observations suggest that NtTTG1 plays an essential role in HCD signal transduction from leaf trichomes to mesophylls. Supplementary material available online at

Tobacco TTG2 Quells Resistance to Pathogens by Sequestering NPR1 from Nuclear Localisation

“…As the WD40 domain has multiple modes for recruiting different substrates, WD40-containing proteins can serve as interchangeable substrate receptors and interact with diverse types of proteins (Xu and Min, 2011). Due to this characteristic, WD40-containing TTG proteins are potential regulators of both plant development and defence pathways (Bouyer et al, 2008;Wang et al, 2009).…”

“…In Arabidopsis, for instance, AtTTG1 interacts with the bHLH transcription factor GL3 while recruiting MYB GL1, thereby forming the WD40-bHLH-MYB complex that acts to regulate trichome development (Morohashi et al, 2007;Szymanski et al, 2000;Zhao et al, 2008). Our previous study showed that WD40 enabled tobacco (Nicotiana tabacum) NtTTG1 to interact with ParA1 (Wang et al, 2009), an elicitin protein that is produced by an oomycete pathogen and induces hypersensitive cell death (HCD) in the plant (Kamoun et al, 1993;Liang et al, 2004). The NtTTG1-ParA1 interaction was essential for the induction of HCD in leaf trichomes (Wang et al, 2009).…”

“…Our previous study showed that WD40 enabled tobacco (Nicotiana tabacum) NtTTG1 to interact with ParA1 (Wang et al, 2009), an elicitin protein that is produced by an oomycete pathogen and induces hypersensitive cell death (HCD) in the plant (Kamoun et al, 1993;Liang et al, 2004). The NtTTG1-ParA1 interaction was essential for the induction of HCD in leaf trichomes (Wang et al, 2009). An NtTTG1-like gene was also cloned from tobacco by amplification with NtTTG1 primers using the polymerase chain reaction (PCR) .…”

“…NtTTG2 differs from NtTTG1 in its organ-specific expression. While ParA1 induces NtTTG1 expression and interacts with the NtTTG1 protein only in the trichome (Wang et al, 2009), NtTTG2 is expressed in the leaves and other organs of the tobacco plant . Because many phytopathogens invade plant leaves rather than trichomes, NtTTG2 is more likely related to pathogen defence than NtTTG1.…”

CsTTG1 Encodes a WD-repeat Protein That Regulates Fruit Wart Formation in Cucumis sativus through Interaction with the Homeodomain-leucine Zipper I Protein Mict

“…The petunia An11, pomegranate (Punica granatum) WD40, Medicago truncatula WD40-1, and maize PAC1 genes, encoding WD-repeat proteins, all control anthocyanin pigmentation and do not regulate trichome development, but they can complement Arabidopsis ttg1 mutant defect in trichomes (de Vetten et al, 1997;Carey et al, 2004;Pang et al, 2009;Ben-Simhon et al, 2011). In addition, the tobacco NtTTG1 protein, a trichome protein with a high degree of sequence identity to AtTTG1, plays an essential role in hypersensitive cell death signal transduction from leaf trichomes to mesophyll cells (Glover et al, 1998;Wang et al, 2009). However, NtTTG2, a paralog of NtTTG1, not only plays a role in suppressing SA/NPR1-regulated defense against pathogens but also regulates development by affecting the expression of ARF genes (Li et al, 2012;Zhu et al, 2013).…”