Stomatal frequency, maturity and index on developing bracts of four abscisic acid mutants and wild-type plants of Arabidopsis thaliana

This study was conducted to determine any relationships between leaf surface features and endogenous levels of abscisic acid (ABA). General growth patterns and various parameters of stomatal location and development were investigated in bracts (cauline leaves) at the onset of flowering of three mutants (abi-1, abi-2, abi-3) of Arabidopsis thaliana (L.) Heynh. insensitive to ABA, one mutant (aba-1) deficient in ABA, and the wild-type (Landsberg) from which the mutants were derived. These ABA mutants have become useful models because they provide an alternative to exogenous application of ABA, thus effectively allowing the study of endogenous ABA activity on plant growth and development. Briefly, plants of the aba-1 mutant were slow growing and dwarf. Bracts were fewer and smaller in abi-1 and abi-2 than the wild-type and abi-3. Stomatal maturity (% stomata with externally visible pores) was higher on the adaxial than the abaxial bract surface for all plant types, and in all mutants than the wild-type. Stomatal maturity was positively correlated with bract age, but not bract area. Stomatal frequency (number of stomata per unit area) was higher on the abaxial bract surface than the adaxial for all plant types. Epidermal cells expanded more quickly on wild-type plants than on the ABA mutants. In aba-1, abi-1, and abi-2 mutants, epidermal cells were small such that stomatal frequency was higher than that of wild-type bracts. Stomatal index [stomatal frequencyx100%/(stomatal frequency+epidermal cell frequency)] was remarkably similar among Landsberg and the four mutants as a result of a relatively constant ratio of epidermal:stomatal frequencies in all plant types. In general, differences among these stomatal parameters were smallest between the wild-type and abi-3. Stomatal features and epidermal-cell growth on bracts of A. thaliana differed between wild-type and mutant plants, yet were similar in three mutants having an insensitivity (abi-1, abi-2) to, or near absence (aba-1) of, endogenous ABA.