Regulation of Apetala2/Ethylene Response Factors in Plants

Abstract

Multiple environmental stresses affect growth and development of plants. Plants try to adapt under these unfavorable condition through various evolutionary mechanisms like physiological and biochemical alterations connecting various network of regulatory processes. Transcription factors (TFs) like APETALA2/ETHYLENE RESPONSE FACTORS (AP2/ERFs) are an integral component of these signaling cascades because they regulate expression of a wide variety of down stream target genes related to stress response and development through different mechanism. This downstream regulation of transcript does not always positively or beneficially affect the plant but also they display some developmental defects like senescence and reduced growth under normal condition or sensitivity to stress condition. Therefore, tight auto/cross regulation of these TFs at transcriptional, translational and domain level is crucial to understand. The present manuscript discuss the multiple regulation and advantage of plasticity and specificity of these family of TFs to a wide or single downstream target(s) respectively. We have also discussed the concern which comes with the unwanted associated traits, which could only be averted by further study and exploration of these AP2/ERFs.

Keywords: AP2/ERF; retrograde regulation; transcriptional regulation; translational regulation; ubiquitination.

Figure 1

miRNA and proteasome mediated regulation of AP2/ERFs. An illustrative model representing the regulation of AP2/ERFs at various levels during multiple stress responses. After onset of stress multiple ERFs are induced and they in turn interact with the cis elements present in the promoter of stress-responsive genes and provide tolerance to various stress. Under normal condition they induce some negative effects like reduced height and senescence that needs to check by indegenous system. Degradation or translational repression by miRNA172 is one example. Other mechanisms include proteasome mediated degradation by different E3 ligases. RGLG interacts with AtERF53 and DRIP interacts with DREB to regulate their expression under normal condition. N-end rule mediated degradation of group VII ERFs under normal (no hypoxia) condition is another mechanism. RAP2.2 and RAP2.4 are also processed for proteasome degradation by SINAT2 and CUL3 ligases. Abbreviations: RGL, RalGDS-like; PRT6, Proteolysis6; SINAT, Seven in absentia 2 of Arabidopsis thaliana; DRIP, DREB2A-interacting protein; RCD1, Radical-induced cell death 1; BPM, BTB/POZ-MATH (bric-a-brac/POX virus and zinc finger—meprin and TRAF homology); RBX1, RING-box protein 1; CUL3, Cullin3; Met AP, methionine aminopeptidase; ATE, arginine transferase; PRT6, Proteolysis 6; RISC, RNA-induced silencing complex.

Figure 2

Clustal and Phylogenetic analysis of DNA binding domain of AP2/ERF. Based on the conserved amino acid sequences present in the DNA binding domain of AP2/ERFs Clustal Omega multiple alignment was generated. Three groups have been considered, one group that binds to both GCC box cis element, one group that binds to DRE cis element and one group that binds to both DRE and GCC cis element. Phylogenetic clustering was done using MEGA6 neighbor joining algorithm. Amino acids that may regulate specific or multiple binding to downstream cis element is also shown.

Figure 3

Retrograde regulation of AP2/ERFs. Abnormalities in plastid leads to induced expression of GUN1, which mediates retrograde signaling to regulate nuclear gene ABI4 and photosynthesis related genes like Lhcb. ABI4 is also regulated by mitochondrial retrograde signaling through mitochondria located RRL protein. RRL regulate expression of AOX1a to further to maintain ROS homeostasis. Another ERF ESE1 interacts physically with Athb21 and ABF4, all of which interact with the COX5b1 promoter to regulate respiratory chain complex. Abbreviations: GUN1, genomes uncoupled-1; PTM, Plant homeodomain type transcription factor with transmembrane domain; phANGs, Photosynthesis associated nuclear genes; CBFA, (CCAAT binding factor A;), ABI4, ABA-INSENTIVE 4; Lhcb, LIGHT HARVESTING COMPLEX B; AOX, Alternative oxidase; ESE1, Ethylene and salt inducible 1; ABF4, ABREbinding factor 4; COX5b1, cytochrome c oxidase subunit 5b-1.