In our recent paper in Journal of Experimental Botany, we examined the effects of cpr5/old1 mutations and CPR5 overexpression on Arabidopsis growth and development. 1 We found that CPR5 is important for early plant growth but promotes senescence at late development and hence proposed it as a senescence-regulatory gene as predicted by the Evolutionary Theory of Senescence derived from studies on animal ageing. One of the key unsolved issues is how CPR5 contributes to the early plant growth and development. Here we discuss the possible cellular functions of CPR5.
The Pleiotropic Phenotypes of cpr5 MutationsCPR5 stands for CONSTITUTIVE EXPRESSER OF PR GENES5. The gene was initially identified in screens for mutants with enhanced disease resistance. 2,3 Several more cpr5 alleles were subsequently identified in screens for mutants with altered trichome development, 4 dark induced senescence (hys1 alleles) 5 and ethyleneinduced senescence (old1 alleles). 1,6 So far, described alterations in cpr5 mutants include (1) enhanced constitutive expression of PR genes, (2) elevated salicylic acid and jasmonic acid levels, (3) hypersensitivities to sugar, ABA, ethylene and jasmonic acid, (4) accelerated leaf senescence, (5) spontaneous lesion mimic cell death, (6) defective cell proliferation, endoreduplication and trichome development, (7) reduced plant growth and reproduction fecundity. 1-7 Thus, cpr5 mutations possess pleiotropic phenotypes indicating that CPR5 is an essential-for-life gene in Arabidopsis.How is CPR5 related to all of these processes? Several double mutants were constructed to dissect how the altered phenotypes in cpr5 mutants are related to the known signalling pathways such as salicylic acid, ethylene, jasmonic acid, sugar and ABA (Jing H-C, Dijkwel PP, unpublished data) 8,9 Blocking glucose sensing by knocking out HXK1 (hexokinase1) could partially alleviate the glucose hypersensitive phenotype of the cpr5 mutant, but did not affect the early onset of senescence and defect in trichome development. 9 This is consistent to our results showing that blocking a particular signalling pathway did not affect the alterations in other signalling pathways in cpr5 mutants. 11 For instance, cpr5-induced ethylene hypersensitivity was converted into ethylene insensitivity in cpr5ein2 double mutants, but cpr5ein2 seedlings still exhibited hypersensitivity to sugar, ABA and jasmonic acid. Similarly, cpr5abi4 double mutants were sugar insensitive but were still hypersensitive to ethylene and jasmonic acid. Furthermore, all examined double mutants so far had no effects on cpr5-induced lesion mimic cell death and premature senescence as well as reduced cell proliferation and trichome development. It appears that CPR5 independently controls multiple cellular processes.
Cellular Functions of CPR5: A Regulator of ROS Gene NetworkThere are at least two possible cellular mechanisms to explain the observed pleiotropy in cpr5 mutants. CPR5 can be a master regulator of a general signal transduction pathway that affects many process...