Amylose-extender dull sugary waxy

Endosperm development in ae du su wx is similar to that in du su wx, with the type-II minor gradient observed and the central endosperm cavity being present by 27 days post-pollination.43 Starch granule and phytoglycogen plastid development in ae du su wx is similar to that in su, except that the quadruple mutant has greater apparent phytoglycogen content at 16 days post-pollination than does su or any other mutant combination.43 However, with development, there is increasing deterioration of the plastids and central endosperm cells.43 

By using mutants of maize and other species, progress has been made in understanding the pathways and enzymes involved in starch biosynthesis and the fine structure of starch polysaccharides. However, starch biosynthesis (Chapter 4) and granule formation are still not completely understood. Thus, integration of the information on polysaccharide biosynthesis (Section 3.6) with that on mutant effects (Section 3.7), is necessary to fully understand polysaccharide biosynthesis and to delineate the limits of this knowledge. 

Genotype Major biochemical changes Enzyme affected 

Interaction of these mutants further clarifies the biosynthetic pathway. For example, the wx mutant is epistatic to all other known maize endosperm mutants and no amylose accumulates (Table 3.6). Mutants such as sh2, bt2 and sit cause major reductions in starch accumulation, but when in combination with wx, the starch produced is all amylopectin.271 In the double mutant ae wx, wx prevents the production of amylose and ae reduces the degree of branching, resulting in the accumulation of a loosely-branched polysaccharide.88 The su mutant is epistatic to du, su2 and wx relative to accumulation of phytoglycogen, but ae and sh2 are partially epistatic to su, causing a marked reduction in the su stimulated phytoglycogen accumulation (Table 3.6). The addition of du or wx to ae su partially overcomes the ae inhibitory effect, and phytoglycogen accumulates. 

Obviously, our understanding of starch biosynthesis is still incomplete, since mutants occur for which the primary metabolic effect has not been determined. Continued evaluation of isozymes and effector compounds, and studies of the in vivo pattern and rate of 14C labeling of intermediates of starch biosynthesis in normal, mutants and mutant combinations should aid in clarifying the nature of the mutations and the pathways of starch biosynthesis. Other aspects of starch formation also remain to be explained. For example, how are starch granules formed as the 

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