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Leslie Sieburth

Associate Professor of Biology

B.S. Humbolt State University

Ph.D. University of Georgia

Research

References

 

 

Research

The goal of our research is to understand the molecular basis for leaf development.  Leaves develop post-embryonically; leaf primordia are small radial structures that arise from a set of stem cells called the shoot apical meristem (SAM), and subsequent growth and differentiation results is a broad flat organ with stereotypical arrangements of specialized cell types.  We use a genetic approach to identify molecules with critical roles controlling leaf development, and are characterizing the molecular and developmental basis for a collection of Arabidopsis leaf mutants generated by our lab.

Novel Long-Distance Signaling Pathway
Characterization of the bypass1 (bps1) mutant led to the surprising discovery that both leaf initiation and leaf development can be actively suppressed from signals arising within the root.  The BYPASS1 gene encodes a novel 349-amino acid plant-specific protein with no functionally-characterized domains.  Because bps1 mutants produce high levels of this root-derived leaf-inhibiting signal, we propose that BPS1 is a negative regulator of a root-to-shoot signaling pathway (Fig 1).  Root-shoot signaling pathways that coordinate plant architecture with environmental signals have been proposed, but molecular components of these signaling pathways are almost unknown.  We are working to understand how the root-derived signal arrests shoot development, to understand how BPS1 regulates production of the signal, and to identify the signal itself.  Using genetic and biochemical approaches, we have determined that the BPS1 signal is a novel carotenoid derivative.

Vesicle Trafficking and Leaf Vein Patterning
In normal leaves, veins form a continuous and interconnected pattern (Fig 2).  In contrast, scarface (sfc) mutants produce leaves with veins largely broken up into isolated vascular fragments that we call vascular islands (Fig 2).  In this mutant, veins initiate as fragmented vascular islands, suggesting that SFC is required early to established a connected pattern..  Using map-based cloning, we identified the SFC gene as an ARF-GAP protein, indicating a role for vesicle trafficking in establishing vein patterning.  We have determined that, in roots, SFC is required for normal endocytic cycling of PIN1, a component of the auxin efflux machinery.  However, our data suggest that SFC affects auxin transport differently in apical tissues.  Three related genes (AGD1, AGD2, and AGD4) also contribute to normal auxin transport.  Current work focuses on the functions of these four ARF GAP proteins in apical tissues.

Leaf Blade Expansion requires RNA decay
Two of our mutants (varicose and trident) that affect cotyledon vein patterning and leaf blade expansion have defects in genes that encode components of the cell’s RNA decay machinery. VARICOSE (VCS) encodes a WD-domain protein and is the ortholog of the human RCD8/GE-1/HEDLS gene.  TRIDENT (TDT) encodes the mRNA decapping enzyme.  Based on a model from metazoans, we expect VCS to function as a scaffold that coordinates RNA decay components, including TDT.  We are currently testing whether TDT and VCS interact in vitro and in planta, identifying additional components of this complex, and characterizing the spectrum of RNA decay processes that are affected in these two mutants.  

 

Figure 1.   BPS1 is a negative regulator of a root-derived long-distance signal that regulates shoot development.

Figure 2.  Cotyledon vein patterns of the wild type, scarface mutant, and the quadruple mutant that combines scarface and mutations in the three related ARF-GAP domain proteins.  Bars=1 mm.

Figure 3.  The trident and varicose mutants show similar seedling and vein pattern defects. Shown are plants that are 11 days and grown at 22 degrees Celsius bars=1 mm.

References