Seed development is intimately dependent upon the metabolic utilization of
sucrose. Our long-term studies have shown that two seed mutants in maize, m
iniature1 (mn1) and shrunken1 (sh1), are caused by mutations in seed-specif
ic genes of sucrose metabolism. A deficiency of the Mn1-encoded cell wall i
nvertase (CWI) enzyme leads to a drastic reduction in seed size identified
as the mn1 seed mutation. We suggest that CWI plays a critical role in prov
iding hexose sugars for mitotic divisions in the early stages of endosperm
development. The CWI also controls endosperm sink strength and developmenta
l stability of the maternal cells in pedicel. The sh1 seed is characterized
by a collapsed crown of the mutant endosperm. The causal basis for the sh1
phenotype is a loss of the Sh1-encoded endosperm-specific sucrose synthase
-l (SSI) which cleaves sucrose to yield precursors for both cellulose and s
tarch biosynthesis. Our recent studies show that the SS1 enzyme plays a pre
dominant role of providing the substrate for cellulose biosynthesis; wherea
s, the second enzyme, SS2, appears to yield precursors for starch biosynthe
sis in a developing endosperm.