| Summary: | Primary plant cell walls are comprised largely of the polysaccharides cellulose,
hemicellulose, and pectins, and can also contain up to 10% protein. These cell wall components
interact non-covalently and covalently to form a functional cell wall. Interactions between
cellulose and pectins are poorly understood, and are the focus of this research. Arabidopsis seed
coat epidermal cells produce three distinct types of cell walls: an outer primary wall; mucilage, a
specialized wall composed primarily of pectins; and a rigid columella. When seeds are hydrated,
mucilage expands rapidly, breaking the outer wall, to form a mucilage halo that surrounds and
remains adherent to the seed. The columella appears to be composed primarily of cellulose, and
is therefore an excellent model for investigating cellulose biosynthesis. Cell wall biosynthesis
and polysaccharide interactions were examined during seed coat development and in mucilage
adherence to better understand cell wall assembly and function.
Cellulose is synthesized by the CELLULOSE SYNTHASE A (CESA) family of
glucosyltransferases. It has been proposed that at least three different CESAs are required to
form a functional Cellulose Synthase Complex (CSC). I investigated the contribution of CESA2,
CESA5 and CESA9 in cellulose biosynthesis during seed coat development. Based on seed coat
epidermal cell morphology and cellulose quantification, all three CESAs have non-redundant
roles in secondary wall biosynthesis, while CESA5 specifically functions in mucilage
biosynthesis. CESA3 is expressed in the seed coat during mucilage biosynthesis and missense
mutations in CESA3, isoxaben resistant 1 (ixr1-1 and ixr1-2), result in altered mucilage structure
and pectin distribution, and reduced cellulose amounts in seeds.
The mechanism of mucilage adherence was examined by comparing two loss of function
mutants that disrupt adherence, cesa5-1 and sos5-2. SOS5 encodes an arabinogalactan protein hypothesized to influence adherence through CESA5. However, the phenotype of each single
mutant differs and a cesa5 sos5 double mutant has an enhanced phenotype. Therefore, it is
unlikely that SOS5 promotes mucilage adherence through CESA5. SOS5 may influence
mucilage structure through galactans, as it is required for the proper function of the !-
galactosidase, MUM2. This demonstrates a role for AGPs in galactan metabolism and cell wall
polysaccharide interactions.
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