SAUR36, a SMALL AUXIN UP RNA Gene, Is Involved in the Promotion of Leaf Senescence in Arabidopsis      

Abstract

Small Auxin Up RNA genes (SAURs) are early auxin-responsive genes, but whether any of them are involved in leaf senescence is not known. Auxin, on the other hand, has been shown to have a role in leaf senescence. Some of the external application experiments indicated that auxin can inhibit leaf senescence, whereas other experiments indicated that auxin can promote leaf senescence. Here, we report the identification and characterization of an Arabidopsis (Arabidopsis thaliana) leaf senescenceassociated gene named SAG201, which is highly up-regulated during leaf senescence and can be induced by 1-naphthaleneacetic acid, a synthetic auxin. It encodes a functionally uncharacterized SAUR that has been annotated as SAUR36. Leaf senescence in transfer DNA insertion saur36 knockout lines was delayed as revealed by analyses of chlorophyll content, F v /F m ratio (a parameter for photosystem II activity), ion leakage, and the expression of leaf senescence marker genes. In contrast, transgenic Arabidopsis plants overexpressing SAUR36 (without its 39 untranslated region [UTR]) displayed an early leaf senescence phenotype. However, plants overexpressing SAUR36 with its 39 UTR were normal and did not exhibit the early-senescence phenotype. These data suggest that SAUR36 is a positive regulator of leaf senescence and may mediate auxin-induced leaf senescence and that the 39 UTR containing a highly conserved downstream destabilizes the SAUR36 transcripts in young leaves.

A Genome-Wide Chronological Study of Gene Expression and Two Histone Modifications, H3K4me3 and H3K9ac, during Developmental Leaf Senescence

“…Auxin synthesis sets in motion major changes in gene expression and physiology (Guilfoyle and Hagen, 2007), and the down-regulation of auxin synthesis and signaling can be considered a primary event in the progression of senescence. Although reports of the role of auxin in leaf senescence conflict (Quirino et al, 1999;Okushima et al, 2005;Hou et al, 2013;Jiang et al, 2014), our molecular data suggest that auxin action is down-regulated during the progression of leaf senescence.…”

A Regulatory Cascade Involving Class II ETHYLENE RESPONSE FACTOR Transcriptional Repressors Operates in the Progression of Leaf Senescence

“…In addition to ESP/ESR, AtERF4 and AtERF8 negatively regulate the expression of many genes, including AUX/IAA genes. Several studies have reported on both the positive and the negative roles of auxin in the progression of leaf senescence (Ellis et al, 2005;van der Graaff et al, 2006;Hou et al, 2013). Because IAA3/ SHY2 suppresses expression of auxin-inducible genes through physical interactions with AUXIN RESPONSE FACTORs (ARFs) and several ARFs act as positive regulators of leaf senescence (Ellis et al, 2005;Weijers et al, 2005), the negative effects on IAA3/SHY2 by AtERF4 and AtERF8 may be involved in the progression of leaf senescence.…”

Arabidopsis SAURs are critical for differential light regulation of the development of various organs

“…Previous studies have shown that ectopic expression of several SAUR family genes resulted in elongated hypocotyls in the light and that plants overexpressing SAUR19 exhibited opened cotyledons in the dark (23)(24)(25). However, several other SAURs have been suggested to inhibit cell expansion in certain organs (26)(27)(28). To test the effects of lirSAURs on plant growth, we generated transgenic lines overexpressing SAUR14, SAUR50, and SAUR65, which were selected to represent classes 1, 2, and 3, respectively.…”

“…Based on microarray analysis, about half of SAURs are up-regulated by auxin treatment in Arabidopsis (22). Overexpression of several distinct SAUR genes resulted in increased growth of cotyledons, hypocotyls, or roots, respectively (23)(24)(25), whereas a few SAURs have been suggested to negatively regulate cell growth in specific organs (26)(27)(28). Recently, it has been found that SAURs could interact with D-clade type 2C protein phosphatase (PP2C) proteins to inhibit their phosphatase activities, therefore activating…”