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- W1577893024 abstract "Cell cycle control is essential for plant growth and development as well as for environmental response (Inze and De Veylder, 2006Inze D. De Veylder L. Cell cycle regulation in plant development.Annu. Rev. Genet. 2006; 40: 77-105Crossref PubMed Scopus (620) Google Scholar). Vegetative growth and development in plants are strongly associated with the extent and proportion of two types of cell cycles: mitosis and endopolyploidization/endocycle. This short article highlights the impact of cell cycle regulation on plant–pathogen interactions and its molecular mechanisms revealed by some recent studies. Alteration of cell cycle progression is observed during plant and pathogen interaction, which reflects either a host defense response or a pathogen-manipulated host susceptible response (Figure 1A). Arabidopsis plants infected with cabbage leaf curl virus have altered expression of cell cycle-associated genes and subsequently an increased ploidy level (Ascencio-Ibanez et al., 2008Ascencio-Ibanez J.T. Sozzani R. Lee T.J. Chu T.M. Wolfinger R.D. Cella R. Hanley-Bowdoin L. Global analysis of Arabidopsis gene expression uncovers a complex array of changes impacting pathogen response and cell cycle during geminivirus infection.Plant Physiol. 2008; 148: 436-454Crossref PubMed Scopus (383) Google Scholar). Golovinomyces orontii, a fungal pathogen causing powdery mildew, promot endocycle at or adjacent to infection sites in Arabidopsis, and an increase in ploidy level in these plant cells may benefit pathogen growth with enhanced nutrient exchange (Chandran et al., 2009Chandran D. Inada N. Hather G. Kleindt C.K. Wildermuth M.C. Laser microdissection of Arabidopsis cells at the powdery mildew infection site reveals site-specific processes and regulators.Proc. Natl. Acad. Sci. USA. 2009; 107: 460-465Crossref PubMed Scopus (143) Google Scholar). This hypothesis is supported by reduced growth of Golovinomyces orontii in the loss of function (LOF) mutant of a transcription factor MYB3R4 that is required for the induction of endocycle at the infection site (Chandran et al., 2009Chandran D. Inada N. Hather G. Kleindt C.K. Wildermuth M.C. Laser microdissection of Arabidopsis cells at the powdery mildew infection site reveals site-specific processes and regulators.Proc. Natl. Acad. Sci. USA. 2009; 107: 460-465Crossref PubMed Scopus (143) Google Scholar). Cell cycle alteration is also observed when bacterial pathogens infect Arabidopsis plants (Hamdoun et al., 2013Hamdoun S. Liu Z. Gill M. Yao N. Lu H. Dynamics of defense responses and cell fate change during Arabidopsis-Pseudomonas syringae interactions.PLoS One. 2013; 8: e83219Crossref PubMed Scopus (21) Google Scholar). Infection by a non-virulent, but not a virulent, bacterial strain or simply treatment with a pathogen-associated molecular pattern (PAMP) signal flg22 resulted in enhanced endocycle and enlarged mesophyll cells in Arabidopsis (Figure 1B). This observation suggests that some effectors from the virulent strain suppress alteration of cell cycle progression from PAMP-triggered immunity (PTI) (Figure 1B). Interestingly, the virulent strain expressing the effector avrRpm1 promotes endocycle and induces large mesophyll cells, suggesting that plants might recognize avrRpm1 and counteract the manipulation of cell cycles by other effectors. The notion that the cell cycle is the battleground between plants and pathogens is further supported by interactome analysis between Arabidopsis proteins and effectors from both bacteria and oomycetes. APC8, a subunit in anaphase-promoting complex/cyclosome (APC/C) that degrades cyclin proteins to promote transitions between cell cycle phases, was identified as one of the five most targeted hub proteins that interact with both pathogen effectors and plant immune regulators (Mukhtar et al., 2011Mukhtar M.S. Carvunis A.R. Dreze M. Epple P. Steinbrenner J. Moore J. Tasan M. Galli M. Hao T. Nishimura M.T. et al.Independently evolved virulence effectors converge onto hubs in a plant immune system network.Science. 2011; 333: 596-601Crossref PubMed Scopus (596) Google Scholar) (Figure 1B). Taken together, host cell cycle progression can be modulated either by plants or pathogens for resistance or pathogenicity (Figure 1A). Some autoimmune mutants were recently found to be defective in cell cycle regulator genes. Cell cycle progression is governed by the activities of cyclin–cyclin-dependent kinase (CDK) complexes, which are negatively regulated by APC/C. OSD1 (Omission of the Second Division 1) and its homolog UVI4 (UV-B-Insensitive 4) inhibit the activity of APC/C through their interaction with activators in APC/C. Both the knockdown mutant of APC10 and transgenic plants overexpressing OSD1 or UVI4 lead to enhanced disease resistance to a virulent bacterial pathogen, Pseudomonas syringae pv. tomato DC3000 (Bao et al., 2013Bao Z. Yang H. Hua J. Perturbation of cell cycle regulation triggers plant immune response via activation of disease resistance genes.Proc. Natl. Acad. Sci. USA. 2013; 110: 2407-2412Crossref PubMed Scopus (45) Google Scholar) (Figure 1C). Enhanced resistance in OSD1 overexpression plants is associated with reduced endocycle, while the osd1 or uvi4 LOF mutants have a higher endocycle and the osd1 uvi4 double mutant is female gametophyte lethal (Bao and Hua, 2014Bao Z. Hua J. Interaction of CPR5 with cell cycle regulators UVI4 and OSD1 in Arabidopsis.PLoS One. 2014; 9: e100347Crossref PubMed Scopus (19) Google Scholar). Intriguingly, a LOF mutant cpr5 (Constitutive expresser of PR genes 5) resembles the OSD1 overexpression plant by having increased disease resistance to virulent bacterial pathogens (Bowling et al., 1997Bowling S.A. Clarke J.D. Liu Y. Klessig D.F. Dong X. The cpr5 mutant of Arabidopsis expresses both NPR1-dependent and NPR1-independent resistance.Plant Cell. 1997; 9: 1573-1584Crossref PubMed Scopus (551) Google Scholar) and a reduced endocycle (Kirik et al., 2001Kirik V. Bouyer D. Schobinger U. Bechtold N. Herzog M. Bonneville J.M. Hulskamp M. CPR5 is involved in cell proliferation and cell death control and encodes a novel transmembrane protein.Curr. Biol. 2001; 11: 1891-1895Abstract Full Text Full Text PDF PubMed Scopus (101) Google Scholar). The ploidy defects in uvi4 and osd1 mutants as well as the lethality of osd1 uvi4 can be inhibited by the cpr5 mutation, suggesting a tight connection between CPR5 and cell cycle regulation. This notion is supported by a recent study showing the complete suppression of enhanced defense responses in the cpr5 mutant by the double LOF mutations of the two CDK inhibitors: SIAMESE (SIM) and SIAMESE-RELATED 1 (SMR1) (Wang et al., 2014Wang S. Gu Y. Zebell S.G. Anderson L.K. Wang W. Mohan R. Dong X. A noncanonical role for the CKI-RB-E2F cell-cycle signaling pathway in plant effector-triggered immunity.Cell Host Microbe. 2014; 16: 787-794Abstract Full Text Full Text PDF PubMed Scopus (72) Google Scholar). Therefore, CPR5 likely has a critical role in the regulation of cell cycle, and perturbation of cell cycle progression is likely the cause of altered defense responses in the cpr5 mutant (Figure 1D). One of the connections between cell cycle progression and defense responses was recently revealed as the expression of plant immune receptor genes coding for nucleotide-binding leucine-rich repeat (NLR) proteins. APC8, a plant–pathogen interaction hub, interacts with nine effectors from the bacterial and the oomycete pathogens (Figure 1B) as well as many Arabidopsis proteins potentially involved in defense responses (Mukhtar et al., 2011Mukhtar M.S. Carvunis A.R. Dreze M. Epple P. Steinbrenner J. Moore J. Tasan M. Galli M. Hao T. Nishimura M.T. et al.Independently evolved virulence effectors converge onto hubs in a plant immune system network.Science. 2011; 333: 596-601Crossref PubMed Scopus (596) Google Scholar). In a reduction of function mutant apc8-1, an NLR gene SNC1 (Suppressor of npr1-1, constitutive 1) had a moderately elevated transcript level (Bao et al., 2013Bao Z. Yang H. Hua J. Perturbation of cell cycle regulation triggers plant immune response via activation of disease resistance genes.Proc. Natl. Acad. Sci. USA. 2013; 110: 2407-2412Crossref PubMed Scopus (45) Google Scholar). Overexpression of OSD1 induces SNC1 expression, which is responsible for its enhanced disease resistance phenotype. Interestingly, a positive regulator of SNC1 expression, MOS1 (Modifier of snc1, 1), is found to be a regulator of endocycle (Bao et al., 2014Bao Z. Zhang N. Hua J. Endopolyploidization and flowering time are antagonistically regulated by checkpoint component MAD1 and immunity modulator MOS1.Nat. Commun. 2014; 5: 5628Crossref PubMed Scopus (33) Google Scholar) (Figure 1C). MOS1 physically interacts with a spindle assembly checkpoint component MAD2 (Mitotic Arrest Deficient 2), and reduces endocycle in an MAD2-dependent manner (Bao et al., 2014Bao Z. Zhang N. Hua J. Endopolyploidization and flowering time are antagonistically regulated by checkpoint component MAD1 and immunity modulator MOS1.Nat. Commun. 2014; 5: 5628Crossref PubMed Scopus (33) Google Scholar). This study suggests a modulation of SNC1 expression through alteration of the cell cycle or co-regulation of cell cycle progression and NLR gene expression by MOS1 (Figure 1C). NLR receptors induce effector-triggered immunity (ETI) including expression of defense-related genes as well as programmed cell death (PCD) (Figure 1C). ETI mediated by NLR immune receptor genes RPS2 and RPP4 are positively regulated by the CDK inhibitors SIM and SMR1 and their target proteins E2F transcription factors (Wang et al., 2014Wang S. Gu Y. Zebell S.G. Anderson L.K. Wang W. Mohan R. Dong X. A noncanonical role for the CKI-RB-E2F cell-cycle signaling pathway in plant effector-triggered immunity.Cell Host Microbe. 2014; 16: 787-794Abstract Full Text Full Text PDF PubMed Scopus (72) Google Scholar) (Figure 1D). SIM and SMR1 might regulate expression of defense response genes because up-regulation of these genes in cpr5 is suppressed by double mutants of SIM and SMR1. In addition, phosphorylation of Retinoblastoma-related 1 (RBR1) is found to be enhanced in NLR-induced defense responses, which could result in overactivation of E2F transcription factors and consequently PCD. These cell cycle regulators also affect PTI but the mechanism remains elusive (Wang et al., 2014Wang S. Gu Y. Zebell S.G. Anderson L.K. Wang W. Mohan R. Dong X. A noncanonical role for the CKI-RB-E2F cell-cycle signaling pathway in plant effector-triggered immunity.Cell Host Microbe. 2014; 16: 787-794Abstract Full Text Full Text PDF PubMed Scopus (72) Google Scholar). Many questions remain to be answered about the connections between pathogen infection, host cell cycle progression, and defense responses. Is perturbation of cell cycle progression during a particular pathogen infection a consequence of a defense response or a pathogen-manipulated response? What host proteins do PAMPs and effectors from pathogens interact with to affect host cell cycle progression? How do different cell cycles affect plant immune responses? Do immunity genes have cell cycle phase-specific expression pattern? Further genetic and genomic studies such as dissection of autoimmune mutants with cell cycle defective and transcriptome profiling at specific phases of the cell cycle will shed more light on the intriguing connection between cell cycle control and plant innate immunity. These studies will enhance our understanding not only of plant–microbe interaction but also of gene regulation associated with cell cycle progression. Research in Hua’s laboratory is funded by NSF IOS-1353738." @default.
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- W1577893024 title "Linking the Cell Cycle with Innate Immunity in Arabidopsis" @default.
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