Common transcriptional regulation of ABA and ethylene

How to cite this article: Valluru R. Common transcriptional regulation of ABA and ethylene. J Plant Sci Phytopathol. 2018; 2: 001-005. https://doi.org/10.29328/journal.jpsp.1001013 Plant hormones are versatile chemical regulators of plant growth. The concept of hormone ‘interaction’ [1] has gained much importance and several key players of hormonal network are uncovered for major plant hormones. The fact that hormones are structurally unrelated and their interaction elicits different genomic and non-genomic responses suggest hormone interaction involve co-regulation at multiple levels [2]. Recent studies suggest that hormonal interaction involves control over biosynthesis genes [3-6], key components of signalling pathways [7,8], hormone distribution [9,10], and interaction at the level of gene expression [11-13]. The spatial and temporal changes in hormone sensitivity add further complexity as they are developmental stagedependent [14]. Understanding how these mechanisms are integrated would allow us to manipulate hormone interaction-regulated growth response under environmental changes. One such prominent emerging hormone interaction is ethylene and abscisic acid (ABA) in several growth processes. In this short review, I discuss some of the common transcriptional regulators of ethylene and ABA.

Plant hormones are versatile chemical regulators of plant growth. The concept of hormone 'interaction' [1] has gained much importance and several key players of hormonal network are uncovered for major plant hormones. The fact that hormones are structurally unrelated and their interaction elicits different genomic and non-genomic responses suggest hormone interaction involve co-regulation at multiple levels [2]. Recent studies suggest that hormonal interaction involves control over biosynthesis genes [3][4][5][6], key components of signalling pathways [7,8], hormone distribution [9,10], and interaction at the level of gene expression [11][12][13]. The spatial and temporal changes in hormone sensitivity add further complexity as they are developmental stagedependent [14]. Understanding how these mechanisms are integrated would allow us to manipulate hormone interaction-regulated growth response under environmental changes. One such prominent emerging hormone interaction is ethylene and abscisic acid (ABA) in several growth processes. In this short review, I discuss some of the common transcriptional regulators of ethylene and ABA.
ABA and ethylene interaction regulates a multitude of plant developmental processes (Table 1). Many developmental processes have been observed to be antagonistically regulated by ABA and ethylene. Plants must therefore need to integrate information provided through ABA-and ethylene-signalling pathways that are largely achieved through transcription factors (TFs), which repress or activate suits of genes to modulate growth responses [15]. Several components identi ied in ABA and ethylene pathways may act as nodes to connect multiple pathways/signals of endogenous developmental and exogenous environmental signals. Recently, these molecular nodes appear to be commonly, often oppositely, regulated by several TFs [4,[16][17][18][19]. Although a plethora of TFs are identi ied as targets of ABA and ethylene signalling [4,[20][21][22][23], here, HD-Zip (homeodomain-leucine zipper), bZIP (basic leucine zipper) and AP2/ERFs (APETALA2/Ethylene Response Factor) that are recently shown to interfere with both ABA and ethylene signalling are discussed. These proteins play roles in regulating plant adaptation under changing environmental conditions [23][24][25] by binding to speci ic DNA sequences and HD-Zip's have the ability to form a large number of interacting complexes affecting hormone-related and developmental functions in vivo [25].
A class 1 HD-Zip TF of tomato, LeHB1, which plays an important role in loral organogenesis and ripening, can transcriptionally activate the expression of tomato LeACO1, a biosynthetic gene of ethylene [24]. LeHB1 binds to LeACO1 promoter sequence with dyad symmetry. Down-regulating LeHB1 via virus-induced gene silencing signi icantly reduced LeACO1 expression, suggesting LeHB1 transcriptionally activate LeACO1 and thus promote ethylene responses [24]. Any ABA interference in LeHB1 overexpressing lines is unknown, however, a Medicago truncatula HD-Zip, MtHB1, acts as a positive regulator of ABA signalling in lateral root emergence [26]. When MtHB1 was overexpressed in the roots, it suppressed LOB-binding domain 1 (LBD1) resulting in longer primary root while reduced lateral root (LR) emergence, which involved MtHB1 repression of auxin-induced ABI3, a ABA-responsive TF, that is important for LR primordia [27] suggesting ABA sensitivity can override auxin response mediated by MtHB1. Interestingly, when ectopically overexpressed, AtHB1 overrides the etiolation response of dark-grown Arabidopsis seedlings [28]. Considering the fact that AtHB1 shares 69% and its HD-Zip domains share 92% similarity to LeHB1 [24] and the triple response is typical to ethylene [29], it is possible that HB1 can act as a positive regulator of ABA response and a negative regulator of ethylene signalling. However, this needs to be experimentally tested.
Ethylene Response Factors of tomato and tobacco, LeERF2 and TERF2, respectively, have shown to involve in the feedback loop of ethylene synthesis [30]. ERF2 belongs to the family of AP2/ERF TFs carrying a single AP2 domain in which acidic N-terminal and/or C-terminal regions act as activation domains [21]. Both LeERF2 andTERF2 activate ethylene biosynthesis genes, ACO and ACS, by binding to GCC box and DRE/ CRT cis-elements and participates in ethylene production. Interestingly, plants overexpressing LeERF2/TERF2 germinated twice as high as that of wild types in the presence of ABA [30]. Similarly, ABA failed to decrease ERF1 expression in an ethylene hypersensitive mutant ctr1 [31]. These studies suggested that ERF1 and ERF2 act as negative regulators of ABA response. However, such negative response was decreased under high ABA levels and salt-induced ERF1 expression was indeed signi icantly lower in ABA-hypersensitive abi1 and abi2 knockout mutants [31], suggesting the dominance of ethylene response over ABA sensitivity might be dependent on ABA levels. Low concentrations of endogenous ABA levels may not necessarily affect ERFs expression, however, under stress conditions, which induces higher ABA levels, ABA or its dominant mutational components might modify ERFs expression and antagonize ethylene responses [31]. Supporting evidence also comes from a dominant negative allele ABI1, which transcriptionally interact and activate a HD-Zip TF of Arabidopsis AtHB6 that act as a negative regulator of ABA inhibition of stomata closure under drought stress [32,33], a reminiscent of ABA-insensitive mutants abi1 and abi2 [34].
These studies highlight the cross-talk between ABA and ethylene responses need further studies using a common experimental platform, where TF promoters carry motifs necessary for binding of genes of both ABA and ethylene pathway. A Helianthus annuus HD-Zip, HaHB4, represent such an excellent resource, which carry two redundant root-speci ic ABA response elements (ABREs, one ABRE is ABA-responsive and the other is NaCl-responsive) and one W-box cis-acting element [16], and is strongly induced by water de icit and ABA [35]. Plants overexpressing HaHB4 was shown to act as a negative regulator of ethylene signalling, while its role in ABA signalling was not reported. Nevertheless, these plants might serve as an excellent resource to study how TFs might regulate both ABA and ethylene signalling in a common experimental platform.
The differential regulation of ABA and ethylene responses is further shown by bZIP TFs. A bZIP factor, HY5 (Long Hypocotyl5) was recently reported to act as a molecular link between ABA and ethylene signalling [4,36]. HY5 was shown to form a part of crucial transcriptional cascade in ABA-modulated ethylene responses. ABA-induced HY5 binds to the G-box of AtERF11 to activate its transcription, which in turn binds to the DRE of, and repress, ACS2 and ACS5 genes, thus attenuating the ethylene biosynthesis [4], suggesting HY5 act as a positive regulator of ABA response and a negative regulator of ethylene response. However, the mechanism how ABAinduced HY5 activates ERF11 is unknown; presumably it may occur through the histone modi ications to ERF11 [37]. Alternatively, given the fact that the ethylene biosynthesis gene (e.g. ACS8) contains cis-element for HY5 binding [38], it is equally possible HY5 could also directly transcriptionally regulate ACS gene expression. Taken together, numerous transcriptional factors appear to be acting as common regulators, but oppositely operating, potentially interfering with both ABA and ethylene signalling pathways.
In addition to TFs, amphipathic helix proteins, SNL1 and SNL2, were recently shown to form another cross-link point of ABA and ethylene signalling [37]. They belong to SWI-INDEPENDENT3 (SIN3)-LIKE protein family, which play roles in recruiting histone binding proteins resulting in a transcriptionally repressed state of the chromatin [39]. During Arabidopsis seed dormancy establishment, SNL1 and SNL2, through histone deacetylation, negatively regulates the ethylene pathway while positively regulates the ABA pathway, leading to an increase in seed dormancy. These two proteins regulate key components of ethylene (ACO1, ACO4, ERF9 and ERF112) and ABA (CYP707A1 & A2, and NCED4) pathway by modifying their histone acetylation levels, thus promoting the seed dormancy [40]. Interestingly, only NCED4 gene expression was down regulated in the double mutant snl1 snl2 (low ABA levels) raising the question whether increased ABA levels would induce SNLs proteins that in turn could repress ethylene signalling is unknown, which deserves further studies.