Final Scientific/Technical report for "ABI8: Prototype of a novel signaling factor"

Finkelstein, Ruth R.¹ 

[1] Univ. of California, Santa Barbara, CA (United States)

关键词: Arabidopsis;    abscisic acid signaling;    sugar signaling;    sugar transport;    cellulose synthesis;    root growth;   

DOI  :  10.2172/1063635
RP-ID  :  DOE/ER15544--2
PID  :  OSTI ID: 1063635

学科分类：生物科学（综合）

美国|英语

来源: SciTech Connect

【 摘 要 】

The Arabidopsis thaliana ABSCISIC ACID-INSENSITIVE8 locus encodes a highly conserved plant-specific protein that mediates abscisic acid (ABA) and sugar responses essential for growth. Although initial database comparisons revealed no domains of predictable function, it has recently been re-annotated as a member of the Glycosyltransferase family A. However, this function has not been demonstrated experimentally and no specific substrates have been identified. Mutations affecting ABI8 are near-lethal due to pleiotropic yet specific effects including altered ABA signaling, sugar transport, cell wall synthesis, root meristem maintenance, vascular patterning, and male sterility. Because the predicted sequence initially provided no clues, we used a guilt by association strategy to address function of this protein by determining its subcellular localization and identifying interacting proteins. Our studies showed that ABI8 is localized to the endomembrane system and may interact with proteins implicated in Golgi trafficking, lignification, and stress signaling. We found that the root meristem arrest reflects decreased auxin accumulation and resulting decreases in regulators required for meristem identity, all of which can be rescued by added glucose. Further studies showed that this glucose-dependence reflects reduced glucose uptake as well as the decreased expression of sugar-mobilizing enzymes. This work suggests that ABI8 may regulate trafficking of membrane proteins such as auxin transporters and cellulose synthase, but this hypothesis has not yet been tested. The altered gene expression is likely to be a secondary or later effect of this pleiotropic mutation.