The absence of debranching enzyme activity and the presence of phytoglycogen in the germinating seeds of sugary1 mutants and commercial sweet corns
--David Pan and Oliver E. Nelson

In an earlier study (Plant Physiol. 74:324-328, 1984), we reported that the sugary1 mutants have reduced debranching enzyme activity in the developing endosperms. The debranching enzymes of nonmutant endosperms can be separated into three fractions on a hydroxyapatite column; the extract of sugary1 endosperms lacks the first fraction; the second and third fractions are also much reduced in activity. In no case is debranching enzyme activity completely absent from sugary1 mutant endosperms. In this note, we report that debranching enzyme activity was not detected in the extract of the germinating seeds of sugary1 mutants nor commercial sweet corns that have sugary1 alleles. As shown in Table 1, the absence of debranching enzyme activity in the germinating seeds of these genotypes is correlated with the presence of phytoglycogen in seed tissues except for the anomalous su1-starchy allele reported by Dahlstrom and Lonnquist (J. Hered. 55:242-246, 1964). While somewhat variable in expression, the homozygous su1-starchy seeds are starchy in appearance. The su1-starchy allele is recessive to the su1 alleles that condition the production of the typical wrinkled seeds. In developing endosperms at 22 DAP, the su1-st endosperms have 56% of the debranching enzyme activity of a Su1 control while other su1 mutants have 9-30% of the control value. Thus, the data of Table 1 are compatible with our previous finding that reduced debranching enzyme activity is correlated with the production of phytoglycogen by developing endosperms. It has been known that the germination rate of sweet corn seeds is usually lower than dent corns. We suggest that the lack of a debranching enzyme activity that would hydrolyze the ,1-6 glycosidic bonds of amylopectin and phytoglycogen would limit their complete degradation during germination and may partially account for the poor germination of sweet corn. The digestion of oligosaccharides extracted from germinating seeds of a su1-R (W64A) mutant and Su1 control with isoamylase and su1-R mutant than nonmutant seeds (Table 2). The evidence supports the hypothesis that debranching enzymes have an important role in degrading amylopectin and phytoglycogen in germinating seeds.

Table 1. The presence of phytoglycogen and the absence of debranching enzyme activity in the germinating seeds of sugary1 mutants and commercial sweet corns.
 

Genotypes	Debranching enzyme activity	Phytoglycogen
Golden Beauty Hybrid	-	+
Wis. Golden 900	-	+
Seneca Chief	-	+
Early Sunglow	-	+
So Sweet	-	+
Tendertreat	-	+
Jubilee	-	+
Sugar Buns	-	+
Mainliner	-	+
Commander	-	+
Silver Treat	-	+
Natural Sweet 9000 (sh2)	+	-
Golden Cross Bantam	-	+
NK 199	-	+
Miracle	-	+
su1-starchy	+	+
W64A su1-R	-	+
Oh43 su1-R	-	+
bt1	+	-
bt2	+	-
sh1	+	-

- not detected
+ presence.

Table 2. Degradation of oligosaccharides extracted from germinating seeds of sugary1 mutant and nonmutant by isoamylase and b-amylase.
 

	% increase in reducing sugar liberated from oligosaccharides after digestion
Enzymes	su1-R (W64A) mutant	Nonmutant
Isoamylase	10.2	7.9
b-amylase	7.4	18.6

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