A leucin zipper domain mediates homo- and heterodimerization between HD-ZIP III factors as well as interaction with the LITTLE ZIPPER proteins, which then block the dimerization and the function. On the molecular level, the expression of HD-ZIP III transcription factors is controlled by miRNA165/166, and the functionality of the proteins is controlled by the interaction with mircoProteins called LITTLE ZIPPER. Moreover, the binding preference of REV to the different binding-sites in the WRKY53 promoter changes during the progression of development and senescence, also indicating an adaptation of the REV properties to certain developmental stages. This is a contradiction that has not yet been solved and points to a more complex scenario. However, on the other hand, WRKY53 expression is induced by increasing levels of hydrogen peroxide, and the REV protein is somehow involved in this response, as the amplitude of this response is dampened in the rev5 mutants. We can already show that the redox state of the REV protein can alter its binding to the WRKY53 promoter, in which the reduced form binds more efficiently to the DNA. One possible explanation could be that REV needs specific modifications or specific interaction partners to act as an activator of WRKY53 expression and senescence. Accordingly, the interaction of REV and WRKY53 appears to be dependent on the developmental stage, and the influence of REV on WRKY53 expression seems to be most efficient at the onset of monocarpic senescence. Vice versa, there is little indication that WRKY53 plays a role in early leaf development and leaf polarity. This can be easily explained by the fact that several other senescence-associated genes (SAGs) are direct targets of REV, as shown by a ChIP-Seq experiment. REV appears to be an important driver for senescence, as the delayed-senescence phenotype of the rev5 mutant is stronger than that of the wrky53 mutant. Chromatin-IP revealed that REV binds directly to the promoter of the senescence-associated transcription factor WRKY53, which is one of the hubs of senescence regulation and is tightly controlled on multiple levels. However, these factors, namely REVOLUTA (REV), not only control these critical steps in early plant development, but are also involved in later steps of development such as leaf senescence and reproduction. Leaf polarity, polarity along the shoot–root axis, and stem cell specification and proliferation are regulated by class III homeodomain leucine zipper (HD-ZIP III) transcription factors. Therefore, REV appears to be under the control of the TIFY family in two different ways: a JA-independent way through TIFY8, which controls REV function in senescence, and a JA-dependent way through PEAPODs and JAZ proteins. Accordingly, REV also interacted with many other members of the TIFY family, namely the PEAPODs and several JAZ proteins in the yeast system, which could potentially mediate the JA-response. Jasmonic acid (JA) had only a limited effect on TIFY8 expression or function however, REV appears to be under the control of JA signaling. ![]() Mutation or overexpression of TIFY8 accelerated or delayed senescence, respectively, but did not significantly alter early leaf development. This interaction inhibited REV’s function as an activator of WRKY53 expression. The interaction between REV and the TIFY family member TIFY8 was confirmed by yeast two-hybrid assays, as well as by bimolecular fluorescence complementation in planta. As this direct regulation appears to be restricted to senescence, we aimed to characterize protein-interaction partners of REV which could mediate this senescence-specificity. REV directly binds to the promoters of senescence-associated genes, including the central regulator WRKY53. The HD-ZIP III transcription factor REVOLUTA (REV) is involved in early leaf development, as well as in leaf senescence.
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