Arabidopsis HOOKLESS1 regulates responses to pathogens and abscisic acid through interaction with MED18 and acetylation of WRKY33 and ABI5 chromatin

Abstract

Arabidopsis thaliana HOOKLESS1 (HLS1) encodes a putative histone acetyltransferase with known functions in seedling growth. Here, we show that HLS1 regulates plant responses to pathogens and abscisic acid (ABA) through histone acetylation at chromatin of target loci. The hls1 mutants show impaired responses to bacterial and fungal infection, accelerated senescence, and impaired responses to ABA. HLS1 modulates the expression of WRKY33 and ABA INSENSITIVE5 (ABI5), known regulators of pathogen and ABA responses, respectively, through direct association with these loci. Histone 3 acetylation (H3Ac), a positive mark of transcription, at WRKY33 and ABI5 requires HLS1 function. ABA treatment and pathogen infection enhance HLS1 recruitment and H3Ac at WRKY33. HLS1 associates with Mediator, a eukaryotic transcription coregulatory complex, through direct interaction with mediator subunit 18 (MED18), with which it shares multiple functions. HLS1 recruits MED18 to the WRKY33 promoter, boosting WKRY33 expression, suggesting the synergetic action of HLS1 and MED18. By contrast, MED18 recruitment to ABI5 and transcriptional activation are independent of HLS1. ABA-mediated priming of resistance to fungal infection was abrogated in hls1 and wrky33 mutants but correlated with ABA-induced HLS1 accumulation. In sum, HLS1 provides a regulatory node in pathogen and hormone response pathways through interaction with the Mediator complex and important transcription factors.

On hormonal regulation of the dynamic apical hook development

“…Genetic and biochemical studies have demonstrated that HLS1 is required for both ethylene‐ and light‐regulated ARF2 protein accumulation, but the underlying molecular mechanism is unclear (Li et al ., ). Consistent with the bioinformatic prediction that HLS1 shows sequence homology with N ‐acetyltransferases (Lehman et al ., ), a recent study has shown decreased levels of histone 3 acetylation at chromosome loci of WRKY33 and ABI5 ( ABA INSENSITIVE 5 ) in hls1 relative to that of the wild‐type (Liao et al ., ). However, direct evidence for the N ‐acetyltransferase activity of HLS1, either in vivo or in vitro , is missing (Liao et al ., ).…”

“…Consistent with the bioinformatic prediction that HLS1 shows sequence homology with N ‐acetyltransferases (Lehman et al ., ), a recent study has shown decreased levels of histone 3 acetylation at chromosome loci of WRKY33 and ABI5 ( ABA INSENSITIVE 5 ) in hls1 relative to that of the wild‐type (Liao et al ., ). However, direct evidence for the N ‐acetyltransferase activity of HLS1, either in vivo or in vitro , is missing (Liao et al ., ). In the light of apical hook development, whether and how this putative N ‐acetyltransferase activity, if it exists, impinges on auxin distribution and signaling remains to be explored (Li et al ., ).…”

The Role and Regulation of ABI5 (ABA-Insensitive 5) in Plant Development, Abiotic Stress Responses and Phytohormone Crosstalk

“…HLS1 and MED18 interact physically and probably are the part of the same complex. Using transgenic Arabidopsis plants it was proved that HLS1 and MED18 are engaged in ABA signaling and are tightly related to ABI5 action (Liao et al, 2016). …”

Manipulation of ABA Content in Arabidopsis thaliana Modifies Sensitivity and Oxidative Stress Response to Dickeya dadantii and Influences Peroxidase Activity

“…This ABA-induced weakening of ROS production should be part of a larger defensive network where ABA acts as a moderating signal. Indeed, transcriptomic and epigenetic studies revealed that ABA down-regulates the expression of many defensive genes (de Torres-Zabala et al, 2007; Cheng et al, 2016; Liao et al, 2016). All these additive effects would explain the extremely susceptible phenotype of the ABA-overproducing plants, even more pronounced than the AtrbohD mutant’s one even if this mutant does not exhibit any oxidative stress response to infection ( Figures 5 , 6 ).…”

“…Recent studies highlighted the major involvement of ABA in the regulation network of plant defense. It induces the accumulation of HLS1, an histone acetyltransferase that regulates epigenetically defense responses (Liao et al, 2016), enhances expression of defense genes through the down-regulation of many miRNAs (Cheng et al, 2016) and its effects on cell wall composition and structure influence resistance to pathogens (Curvers et al, 2010; Sánchez-Vallet et al, 2012). All these data would explain the negative impact of ABA on pathogen defense in some pathosystems (Asselbergh et al, 2008b).…”