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  • The importance of AAE in enhancing the survival of plants

    2019-08-13

    The importance of AAE3 in enhancing the survival of plants and yeast when confronted with certain environmental stresses has been documented in recent reports. In response to biotic stress such as oxalate-secreting micro-organisms, AAE3 was found to reduce the inhibitory growth effects of the secreted oxalate on yeast [2]. In plants, AAE3 was determined to reduce the susceptibility of plants to oxalate-secreting phytopathogens [1,3,7]. In addition, two studies utilizing different plant species reported the importance of AAE3 in regulating aluminum tolerance [[4], [5], [6]]. An interesting aspect of these two latter studies is that in one report, a reduction in AAE3 resulted in a decrease in aluminum sensitivity [5], while in the other report, an increase in AAE3 resulted in a decrease in aluminum sensitivity [4]. This apparent discrepancy will need to be clarified with additional studies before any firm conclusion can be drawn. Thus far, the importance of AAE3 in plant growth has been confined to a single report in Arabidopsis [1]. Characterization of an Ataae3 T-DNA mutant showed that lack of AAE3 cyp3a inhibitors resulted in reduction in vegetative growth, seed mucilage production, seed germination, and an increase in calcium oxalate accumulation in Arabidopsis. Whether such phenotypes are specific to Arabidopsis or whether a reduction in AAE3 expression would result in similar phenotypes in other plants remains unknown. To expand our understanding of the impact of AAE3 in plant growth and development, we report here the characterization of Mtaae3 RNAi knock-down and Mtaae3 Tnt1 knock-out mutants. Comparisons of these determined phenotypes to the Ataae3 mutants provide additional insights into the responsiveness of each developmental phenotype to changes in the level of AAE3 gene expression. Like the Ataae3 T-DNA knock-out mutant, the Mtaae3 RNAi knock-down mutant showed an increase in calcium oxalate accumulation but lacked other Ataae3 mutant phenotypes. This apparent discrepancy was clarified through the phenotypic characterization of a Mtaae3 Tnt1 knock-out mutant, which displayed phenotypes similar to Ataae3 T-DNA knock-out mutant. These findings show that the level of AAE3 gene expression is important in determining the severity of the exhibited phenotypes.
    Materials and methods
    Results and discussion
    Acknowledgements The contents of this publication do not necessarily reflect the views or policies of the U.S. Department of Agriculture, nor does mention of trade names, commercial products, or organizations imply endorsement by the U.S. Government. This work was supported by the U.S. Department of Agriculture, Agricultural Research Service, under Cooperative agreement number 58-3092-5-001. Development of M. truncatula Tnt1 insertion lines and reverse genetics screenings were supported by National Science Foundation, USA (DBI 0703285 & IOS-1127155) and The Noble Research Institute.
    Introduction Aberrations in post-translational modifications by ubiquitin or ubiquitin-like proteins (Ubl), such as the small ubiquitin-like modifiers (SUMO), are associated with the pathogenesis of life-threatening diseases, such as cancer (Sarge and Park-Sarge, 2011, Zhu et al., 2010), neurodegenerative disorders (Steffan et al., 2004, Subramaniam et al., 2009), and viral infection (Jaber et al., 2009, Kim et al., 2010). For example, multiple studies indicate that SUMOylation is dysregulated in many types of cancers and that the SUMO-activating enzyme (SAE, SUMO E1) could be a potential target to cyp3a inhibitors inhibit c-Myc- and KRas-dependent oncogenesis (He et al., 2017, Kessler et al., 2012, Luo et al., 2009, Yu et al., 2015) and reduce cancer cell stemness and resistance (Bogachek et al., 2016, Du et al., 2016). The activating enzyme catalyzing ubiquitin-like Atg8 and Atg12 modifications in autophagy, known as Atg7, has been shown as an indirect target for KRas-dependent oncogenesis (Guo et al., 2013, Rosenfeldt et al., 2013). Despite the importance of Ubl modifications in dysregulated signaling pathways in diseased cells, only a handful of U.S. Food and Drug Administration-approved drugs targeting this type of post-translational modifications have been developed. This deficiency illustrates knowledge gaps in targeting these enzymes by small molecules and underscores the need to discover novel chemotypes and mechanisms to inhibit Ubl modifications.