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AtDeg2 is a chloroplast protein with dual protease/chaperone activity. Since data on how the individual activities of AtDeg2 affect growth and development of Arabidopsis thaliana plants is missing, two transgenic lines were prepared that express mutated AtDeg2 versions that have either only protease or chaperone activity and a comprehensive ontogenesis stage-based study was performed comprising wild type (WT) plants and insertional mutants that do not express AtDeg2, as well as the two transgenic lines. The repression of both AtDeg2 activities in deg2-3 mutants altered just a few phenotypic traits including the time when cotyledons were fully opened, the time when 10% flowers were open as well as the number of inflorescence branches and seed length in plants which have completed their generative development. It was demonstrated that complete opening of cotyledons as well as the number of inflorescence branches and seed length in plants which have completed their generative development required involvement of both AtDeg2 activities, whereas the time when 10% of flowers were open was controlled by AtDeg2 protease activity. These results show for the first time that the chaperone activity of AtDeg2 is needed for some elements of generative development of A. thaliana plants to proceed normally. So far, the chaperone activity of AtDeg2 was confirmed based on in vitro assays only.

The chloroplast protein AtDeg5 is a serine-type protease peripherally attached to thylakoid membrane at its lumenal side. Since reliable data regarding the role of AtDeg5 in controlling the course of growth and developmental processes are extremely limited, two independent T-DNA insertional lines with different extent of AtDeg5 reduction were prepared and ontogenesis stage-based analysis performed. Both mutant lines displayed a compensatory overaccumulation of AtDeg8. The repression of AtDeg5 protease altered a range of phenotypic features in at least one of the mutants, with the most prominent being changes in chronological progression of development and growth of individual rosette leaves, flower production and silique ripening as well as in the area of fully expanded leaves and chloroplast ultrastructure. By analyzing the results of parallel-mutant screening we conclude that AtDeg8 overdose may rescue 23% of AtDeg5 deficiency with regard to some AtDeg5-controlled traits; alternatively AtDeg5 may have catalytic sites in excess so that these traits might remain unaltered when AtDeg5 pool is reduced by 23%. For some other AtDeg5-dependent traits the absence of excessive amount of AtDeg5 catalytic sites, lack of AtDeg5 dosage effect and inability of AtDeg8 to compensate deficiency or absence of AtDeg5 occurred.