ABSTRACT
We have isolated a gene, AtPer1, from the dicotyledon Arabidopsis thaliana, which shows similarity to the 1-cysteine (1-Cys) peroxiredoxin family of antioxidants. In higher plants, members of this group of antioxidants have previously only been isolated from monocotyledons. It has been suggested that seed peroxiredoxins protect tissues from reactive oxygen species during desiccation and early imbibition and/or are involved in the maintenance of/protection during dormancy. AtPer1 expression is restricted to seeds. Despite differences in seed development between monocots and dicots, AtPer1 shows an expression pattern during seed development and germination similar to the dormancy-related transcript Per1 in barley. In situ hybridization identifies AtPer1 as the first aleurone-expressed transcript characterized in developing Arabidopsis seeds. The transcript is also expressed in the embryo. AtPer1 expression in seeds is unaltered in an ABA-deficient mutant (aba-1) during seed development, while expression in seeds of an ABA-insensitive mutant (abi3-1) is reduced. The transcript is not induced in vegetative tissue in response to stress by ABA or drought. AtPer1 transcript levels are correlated to germination frequencies of wildtype seeds, but AtPer1 transcript abundance is not sufficient for expression of dormancy in non-dormant mutants. Hypotheses on peroxiredoxin function are discussed in view of the results presented here.
Subject(s)
Antioxidants/metabolism , Arabidopsis Proteins , Arabidopsis/genetics , DNA, Plant/isolation & purification , Plant Proteins/biosynthesis , Amino Acid Sequence , Arabidopsis/metabolism , Base Sequence , Blotting, Southern , DNA, Plant/chemistry , Gene Expression Regulation, Plant , Germination/genetics , Molecular Sequence Data , Plant Proteins/genetics , Polymerase Chain Reaction , Seeds/genetics , Sequence AlignmentABSTRACT
Ameloblastic disturbances are correlated with defects in enamel. Experimental disturbances created by tetracyclines, fluorides, and antimitotic drugs are emphasized. Cellular alterations are shown to interfere with both matrix production and secretion. Defects in enamel formation are characterized by abnormal crystal size and distribution. Further research in normal and particularly abnormal enamel development is needed to establish: 1. exact mode of matrix secretion and its relation to crystal nucleation and orientation 2. function of maturative ameloblast and its relation to the stratum intermedium and papillary layer during that phase 3. cause for lack of mineralization of matrix, particularly in ectopic areas.
