NOVEMBER 5-9, 2000    KANSAS CITY, MISSOURI

A A C C   2 0 0 0   A n n u a l   M e e t i n g

314
Discovery of five additional hardness mutations in the puroindoline b gene sequence of hexaploid wheat.
C. F. MORRIS (1), M. C. Simeone (1), and M. Lillemo (2). (1) USDA-ARS Western Wheat Quality Lab., Pullman, WA 99164; (2) Dep. Horticulture & Crop Sci., Agric. Univ. Norway, As, Norway.

Grain hardness in wheat results from the loss of puroindoline gene function. In its natural, "wild-type" state, wheat grain is soft; hardness arises through the loss of puroindoline a or b protein (null mutations), or the alteration of puroindoline b protein sequence (point mutations). Currently, seven hardness mutations have been characterized and in all cases one puroindoline is affected whereas the other remains wild-type. From this, a model of puroindoline gene function suggests that both proteins are necessary to effect a full level of grain softness. These five new alleles have been provided the molecular loci designations of Pinb-D1c through Pinb-D1g. Pinb-D1c is relatively prevalent, whereas the other four alleles are represented by only eight known varieties and their progenitors. The last three mutations all involve generation of a "stop" codon and a lack of puroindoline b protein (nulls). A complete description of the molecular genetics of puroindoline grain hardness will be presented with the progress of backcrossing all hardness alleles into a common background.

 


Copyright © 2000
American Association of Cereal Chemists, Inc.
all rights reserved