Abstract
The impact of cell cycle on plant immunity was indicated by the enhancement of disease resistance with overexpressing OSD1 and UVI4 genes that are negative regulators of cell cycle controller APC (anaphase promoting complex). CPR5 is another gene that is implicated in cell cycle regulation and plant immunity, but its mode of action is not known. Here we report the analysis of genetic requirement for the function of UVI4 and OSD1 in cell cycle progression control and in particular the involvement of CPR5 in this regulation. We show that the APC activator CCS52A1 partially mediates the function of OSD1 and UVI4 in female gametophyte development. We found that the cpr5 mutation suppresses the endoreduplication defect in the uvi4 single mutant and partially rescued the gametophyte development defect in the osd1 uvi4 double mutant while the uvi4 mutation enhances the cpr5 defects in trichome branching and plant disease resistance. In addition, cyclin B1 genes CYCB1;1, CYCB1;2, and CYCB1;4 are upregulated in cpr5. Therefore, CPR5 has a large role in cell cycle regulation and this role has a complex interaction with that of UVI4 and OSD1. This study further indicates an intrinsic link between plant defense responses and cell cycle progression.
Highlights
Regulation of cell cycle, in the form of meiosis, mitosis, and endoreduplication, is critical for plant growth and development [1,2,3,4]
The osd1-2 mutant in Landsberg erecta (Ler) had a significant increase of the number of 16C and 32C cells compared to wild-type Ler (Figure 1A)
Similar to previous report [38], we found that the female gametophyte development in osd1 uvi4 is arrested at FG1 stage and the megaspore cannot complete mitosis to develop into a functional female gametophyte (Figure S1)
Summary
Regulation of cell cycle, in the form of meiosis, mitosis, and endoreduplication, is critical for plant growth and development [1,2,3,4]. Progression through cell division cycles is governed by activities of cyclin-dependent kinase (CDK)-cyclin complexes which are bound and activated by cyclins at specific cell cycle phases. Activities of CDKs are relatively high at G1/S and G2/M transition phases where a large number of proteins are phosphorylated to promote the onset of DNA replication and mitosis respectively. The activity of mitotic CDK-cyclin complex at the G2/ M transition phase needs to be repressed, which could be achieved by activation of the anaphase-promoting complex/cyclosome (APC/C). Arabidopsis has five CDC20 homologs (CDC20.1 to CDC20.5) and three CDH1 homologs (CCS52A1, CCS52A2, and CCS52B) Both CCS52A1 and CCS52A2 are reported to regulate the onset of endoreduplication, but the function of CCS52B is largely unknown [8,9,10,11]
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