-
Categories
-
Pharmaceutical Intermediates
-
Active Pharmaceutical Ingredients
-
Food Additives
- Industrial Coatings
- Agrochemicals
- Dyes and Pigments
- Surfactant
- Flavors and Fragrances
- Chemical Reagents
- Catalyst and Auxiliary
- Natural Products
- Inorganic Chemistry
-
Organic Chemistry
-
Biochemical Engineering
- Analytical Chemistry
-
Cosmetic Ingredient
- Water Treatment Chemical
-
Pharmaceutical Intermediates
Promotion
ECHEMI Mall
Wholesale
Weekly Price
Exhibition
News
-
Trade Service
Editor-in-Chief | Wang Yi On February 8, 2022, Wang Shui's research group from Shanghai Normal University published a research titled CONSTITUTIVE EXPRESSER OF PATHOGENESIS-RELATED GENES 5 is an RNA-binding protein controlling plant immunity via an RNA processing complex online in The Plant Cell thesis
.
CPR5 (CONSTITUTIVE EXPRESSER OF PATHOGENESIS-RELATED GENES 5) is a negative regulator of plant immunity that was cloned through genetic screening 25 years ago (Bowling et al.
, Plant Cell, 1997)
.
Except for the C-terminal with 4-5 transmembrane domains, the protein does not contain domains with known functions, which greatly hinders its in-depth study
.
This study found that CPR5 is an SR family RNA-binding protein that regulates plant immunity through the RNA processing complex
.
The ability of plants to overcome a wide variety of and constantly changing pathogenic microorganisms demonstrates the plasticity of the plant innate immunity system
.
RNA processing is an important way to increase the diversity of signaling molecules
.
CPR5 links the two basic life processes of RNA processing and plant immunity, laying a theoretical foundation for revealing the mechanism of plant immune plasticity regulation
.
The immune system is divided into adaptive immune system and innate immune system
.
The receptor genes of the adaptive immune system come from specialized immune cells, and unlimited receptor genes are generated by homologous recombination of somatic DNA, while the receptor genes of the innate immune system come from germ cells, and the number is limited and inexhaustible.
changed
.
Plants only have an innate immune system, and the number of immune receptor genes in plants whose genomes have been sequenced so far are very limited.
For example, the Arabidopsis and rice genomes contain ~200 and ~500 NLR immune receptor genes, respectively
.
How do plants cope with a wide variety of ever-mutating pathogenic microorganisms with such a small number of receptor genes? So far it remains a mystery
.
The plant innate immune system is divided into two levels: pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI) and effector-triggered immunity (ETI)
.
After pathogenic microorganisms infect plants, on the one hand, the receptor PRR on the plasma membrane of the plant recognizes PAMP and activates the plant PTI through the MAPK signaling pathway; on the other hand, the NLR receptor in the plant cell recognizes the effector and triggers a stronger immune response than PTI.
ETI, Often accompanied by programmed cell death (PCD), also known as hypersensitivity (HR)
.
Recent studies have found that plant PRR receptors and NLR receptors synergistically regulate plant immunity, and the activated NLR receptors form a resistance body.
So far, the signaling pathway downstream of NLR receptors to activate plant ETI is still unclear
.
Plant NLR receptors are mainly divided into two types: CC-NLR and TIR-NLR, whose downstream signals are transmitted by NDR1 and EDS1, respectively
.
At present, the research on EDS1 is relatively in-depth.
After pathogenic microorganisms infect plants, they form an EDS1/effector/NLR receptor complex and shuttle between the nucleocytoplasm
.
The complex promotes ETI in the nucleus and PCD in the cytoplasm, suggesting that the nuclear envelope plays an important role in regulating ETI in plants
.
To study the molecular mechanism of plant ETI, two types of mutants can be utilized: one is an NLR receptor-autonomously activated mutant, and the other is a PCD-autonomously activated necrosis-like mutant (LLM)
.
Among the NLR receptor autonomous activation mutants, the most studied is the snc1 (suppressor of npr1, constitutive 1) mutant
.
SNC1 is a TIR-NLR receptor because an amino acid change (glutamate-lysine) between the NBS and LRR domains allows the mutated protein to activate autonomously without the need for an effector
.
By screening the snc1 mutant suppressor mos (modifier of snc1), two important signaling pathways were found to be involved in the regulation of plant ETI: (1) nucleocytoplasmic transport signaling pathways, including nucleoporins MOS3 and MOS7, nuclear import proteins MOS6 and MOS14 , and the nucleocytoplasmic RNA transport protein MOS11; (2) RNA processing signaling pathways, including RNA splicing and modification proteins MOS2, NTC complex and MOS12
.
Through extensive genetic screening, some necrosis-like mutants (LLMs) with autonomously activated PCD have been found, which are divided into two categories: the first category of LLM mutants determines the initiation of PCD, such as cpr5, acd6 and ssi1, etc.
; the second category of LLMs Mutants control the strength of PCD, such as lsd1 and acd1,
etc.
The function of these proteins and the molecular mechanism of regulation between them are still unclear
.
cpr5 is an LLM mutant obtained by screening Arabidopsis cpr (constitutive expressor of pathogenesis-related genes) using the plant defense reporter gene PR2:GUS.
It has autonomously activated immunity and a phenotype similar to HR necrosis
.
RNA-seq analysis of wild-type and cpr5 mutant plants revealed that differentially expressed genes (DEGs) regulated by CPR5 overlapped 74.
9% with plant ETI-related DEGs, while only about 11.
2% overlapped with plant PTI-related DEGs, indicating that CPR5 mainly Involved in the regulation of plant ETI
.
By analyzing the CPR5 signaling pathway, three important signaling pathways were found to be involved in the regulation of plant ETI: (1) Cell cycle signaling pathway
.
The core signaling regulatory chain of the cell cycle, CKI-RB-E2F, activates plant ETI downstream of CPR5 (Wang et al.
, Cell Host & Microbe, 2014)
.
(2) Nucleocytoplasmic transport signaling pathway
.
CPR5 is a novel nucleoporin that normally forms homodimers, binds the core cell cycle regulator CKI and inhibits the nucleocytoplasmic trafficking of immune signaling molecules
.
After the plant is infected by pathogenic bacteria, the activated NLR receptor changes the conformation of CPR5, depolymerizes its dimer into monomer, releases CKI on the one hand, and opens the nuclear-cytoplasmic transport of immune signaling molecules on the other hand.
Plant ETI (Figure 1) (Dasso and Fontoura, Cell, 2016; Gu et al.
, Cell, 2016)
.
(3) RNA processing signaling pathway
.
Genetic analysis found that the RNA splicing factor NTC and the RNA poly(A) tailing factor CPSF synergistically activate plant ETI downstream of CPR5 (Peng et al.
, Plant Cell, 2022)
.
Therefore, genetic analysis of both SNC1 and CPR5 signaling reveals that plant ETI is regulated by two basic life processes, nucleocytoplasmic transport and RNA processing
.
Figure 1 After activation of the NLR receptor, the conformation of the nucleoporin CPR5 is changed.
On the one hand, it opens the nuclear pore to promote the transport of immune signaling molecules into the nucleus, and on the other hand, it releases the cell cycle core regulator CKI.
Companion PCD (adapted from Dasso and Fontoura, Cell, 2016)
.
Although most genes in the plant genome are regulated by RNA processing, such as the Arabidopsis genome, 61% of genes have RNA alternative splicing and 75% have RNA variable poly(A) tailing, so far the regulation of RNA processing Very little is known about plant immunity
.
NTC is an activator of the RNA spliceosome and consists of eight core proteins, including Prp19, CDC5L, PRL1, AD-002, SPF27, DAM1, CTNNBL1 and HSP73
.
Four of these members, Prp19, CDC5L, PRL1 and SPF27, have been found to activate plant immunity downstream of SNC1
.
In the process of plant immunity, some NLR genes undergo RNA alternative splicing, such as N gene of tobacco, RPS4 gene and SNC1 gene of Arabidopsis
.
NLR family genes may be hotspot target genes for RNA alternative splicing, the average transcript of Arabidopsis genome-wide genes is about 2.
40, while the average transcript of NLR family genes is about 3.
38
.
Some effectors of pathogenic microorganisms can directly bind to RNA splicing factors to regulate plant immunity
.
For example, HopU1 is an ADP glycosyltransferase that glycosylates two arginine residues in the RNA-binding domain RRM of GRP7 protein, blocking GRP7 from binding to the transcripts of the PRR receptors FLS2 and EFR genes on the surface of plant cells, thereby inhibiting plant growth.
PTI
.
In addition to alternative splicing, RNA variable poly(A) tailing also regulates plant immunity, particularly the CPR5 signaling pathway
.
The RNA poly(A) tailed complex contains PAPS, CPSF, CFIm, CFIIm and CSTF
.
The CPSF complex in turn contains CPSF160, CPSF100, CPSF73, CPSF30, FIP1 and WDR33
.
Arabidopsis thaliana contains 4 PAPS genes
.
PAPS1 is a negative plant immune regulator
.
Autonomously activated immune responses in paps1 mutants can be suppressed by eds1 or pad4
.
RNA-seq analysis showed that the DEGs of the paps1 mutant and the DEGs of the cpr5 mutant mostly overlapped
.
CPSF30 is a core member of the CPSF complex
.
cpsf30 mutants inhibit cell death in cpr5, lsd1 and mpk4 mutants
.
The Shui Wang team found through genetic screening that PRL1 and FIP1 activate plant immunity downstream of CPR5
.
PRL1 and FIP1 are core members of the RNA splicing factor NTC complex and the RNA poly(A) tailing factor CPSF complex, respectively
.
Further genetic analysis of other core factors of both complexes showed that both the entire NTC complex and the CPSF complex activate plant immunity downstream of CPR5
.
Analyses using BiFC-YFP, Co-IP and FRET-FLIM showed that CPR5, PRL1 and FIP1 formed a complex that co-localized in the nuclear speck of RNA-processing organelles
.
Through sequence comparison and functional substitution of different plant proteins, it was found that CPR5 is an RNA-binding protein of the Tra2 subfamily of the SR family
.
The Tra2 subfamily is a class of atypical SR family proteins with SR-RRM domains arranged in order (the RNA recognition domain RRM is arranged after the SR domain)
.
A typical SR family protein has an RRM-SR domain arrangement (RRMs are arranged before SR domains)
.
RNA-seq analysis identified 473 RNA alternatively spliced genes (ASGs) regulated by CPR5
.
AGO1 is one of these ASGs, and ago1 mutants can suppress cpr5 mutant immune responses and PCD phenotypes, suggesting that AGO1 activates plant immunity downstream of CPR5
.
Therefore, our study revealed: 1) CPR5 is an SR family RNA-binding protein; 2) The RNA splicing factor NTC and the RNA poly(A) tailing factor CPSF coordinately regulate plant immunity; 3) CPR5 links RNA processing and plant immunity Large basic life processes are linked (Figure 2)
.
Figure 2 CPR5 regulates plant immunity through the RNA splicing factor PRL1 and the RNA poly(A) tailing factor FIP1
.
(A) PRL1 (SCPR44) and FIP1 (SCPR57) activate PCD downstream of CPR5 (arrows indicate cotyledon premature senescence)
.
(B) PRL1 and FIP1 cooperatively regulate plant ETI (left) and basal immunity (right)
.
(C) BiFC-YFP analysis of CPR5, SR34, PRL1 and FIP1 subcellular colocalization
.
SR34, indicates nuclear spot location; mCherry-NLS, indicates nuclear spot location; NS, nuclear spot
.
(D) SR domain at the N-terminus of CPR5 protein, sequence comparison of different plant CPR5 proteins
.
(E) Schematic diagram of the protein structure (SR, RRM and TM domains) of the SR family Tra2 subfamily (including human RNPS1 and Arabidopsis CPR5, SR45 and SR45a proteins) (from Peng et al.
, Plant Cell, 2022)
.
In recent years, a series of studies by Wang Shui's team to analyze the regulatory pathway of CPR5 signaling revealed that CPR5, as an SR family RNA-binding protein, is the first immune signaling factor discovered so far, integrating the three basic elements of nucleocytoplasmic transport, cell cycle and RNA processing.
Life processes are integrated to regulate plant immunity (Figure 3) (Wang et al.
, Cell Host & Microbe, 2014; Gu et al.
, Cell, 2016; Peng et al.
, Plant Cell, 2022)
.
Therefore, cpr5 mutants will be an important genetic tool for dissecting ETI signaling in plants
.
Figure 3 CPR5 is an RNA-binding protein that is both a member of the nuclear pore complex (NPC) and a member of the nuclear speck
.
On the one hand, the activated NLR receptor changes the conformation of CPR5 protein, promotes the transport of immune signaling molecules into the nucleus, and releases the core cell cycle regulator CKI at the same time
.
On the other hand, CPR5 forms a complex with NTC/CPSF in the nuclear speck.
The immune signaling factors in the nucleus and CKI work together to relieve the inhibition of CPR5 on the NTC/CPSF complex, regulate RNA alternative splicing, and form transcripts encoding full-length or partial proteins.
, the ratio of the two regulates the balance between plant immunity and development
.
Peng Shun, a doctoral student from the School of Life Sciences, Shanghai Normal University, and Guo Dongbei and Guo Yuan, postgraduate students, are the co-first authors of the paper, and researcher Wang Shui is the corresponding author of the paper
.
Professor Cai Yingfan from the School of Life Sciences of Henan University and Chen Dong from Wuhan Ruixing Biotechnology Co.
, Ltd.
participated in the research of this paper
.
The research was funded by the National Natural Science Foundation of China, the Shanghai Plant Germplasm Resources Engineering Technology Research Center, and the Shanghai Key Laboratory of Plant Molecular Biology
.
Link to the original text of the Wang Shui research group (the first from the right in the second row is Wang Shui researcher): https://academic.
oup.
com/plcell/advance-article/doi/10.
1093/plcell/koac037/6524637#
.
CPR5 (CONSTITUTIVE EXPRESSER OF PATHOGENESIS-RELATED GENES 5) is a negative regulator of plant immunity that was cloned through genetic screening 25 years ago (Bowling et al.
, Plant Cell, 1997)
.
Except for the C-terminal with 4-5 transmembrane domains, the protein does not contain domains with known functions, which greatly hinders its in-depth study
.
This study found that CPR5 is an SR family RNA-binding protein that regulates plant immunity through the RNA processing complex
.
The ability of plants to overcome a wide variety of and constantly changing pathogenic microorganisms demonstrates the plasticity of the plant innate immunity system
.
RNA processing is an important way to increase the diversity of signaling molecules
.
CPR5 links the two basic life processes of RNA processing and plant immunity, laying a theoretical foundation for revealing the mechanism of plant immune plasticity regulation
.
The immune system is divided into adaptive immune system and innate immune system
.
The receptor genes of the adaptive immune system come from specialized immune cells, and unlimited receptor genes are generated by homologous recombination of somatic DNA, while the receptor genes of the innate immune system come from germ cells, and the number is limited and inexhaustible.
changed
.
Plants only have an innate immune system, and the number of immune receptor genes in plants whose genomes have been sequenced so far are very limited.
For example, the Arabidopsis and rice genomes contain ~200 and ~500 NLR immune receptor genes, respectively
.
How do plants cope with a wide variety of ever-mutating pathogenic microorganisms with such a small number of receptor genes? So far it remains a mystery
.
The plant innate immune system is divided into two levels: pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI) and effector-triggered immunity (ETI)
.
After pathogenic microorganisms infect plants, on the one hand, the receptor PRR on the plasma membrane of the plant recognizes PAMP and activates the plant PTI through the MAPK signaling pathway; on the other hand, the NLR receptor in the plant cell recognizes the effector and triggers a stronger immune response than PTI.
ETI, Often accompanied by programmed cell death (PCD), also known as hypersensitivity (HR)
.
Recent studies have found that plant PRR receptors and NLR receptors synergistically regulate plant immunity, and the activated NLR receptors form a resistance body.
So far, the signaling pathway downstream of NLR receptors to activate plant ETI is still unclear
.
Plant NLR receptors are mainly divided into two types: CC-NLR and TIR-NLR, whose downstream signals are transmitted by NDR1 and EDS1, respectively
.
At present, the research on EDS1 is relatively in-depth.
After pathogenic microorganisms infect plants, they form an EDS1/effector/NLR receptor complex and shuttle between the nucleocytoplasm
.
The complex promotes ETI in the nucleus and PCD in the cytoplasm, suggesting that the nuclear envelope plays an important role in regulating ETI in plants
.
To study the molecular mechanism of plant ETI, two types of mutants can be utilized: one is an NLR receptor-autonomously activated mutant, and the other is a PCD-autonomously activated necrosis-like mutant (LLM)
.
Among the NLR receptor autonomous activation mutants, the most studied is the snc1 (suppressor of npr1, constitutive 1) mutant
.
SNC1 is a TIR-NLR receptor because an amino acid change (glutamate-lysine) between the NBS and LRR domains allows the mutated protein to activate autonomously without the need for an effector
.
By screening the snc1 mutant suppressor mos (modifier of snc1), two important signaling pathways were found to be involved in the regulation of plant ETI: (1) nucleocytoplasmic transport signaling pathways, including nucleoporins MOS3 and MOS7, nuclear import proteins MOS6 and MOS14 , and the nucleocytoplasmic RNA transport protein MOS11; (2) RNA processing signaling pathways, including RNA splicing and modification proteins MOS2, NTC complex and MOS12
.
Through extensive genetic screening, some necrosis-like mutants (LLMs) with autonomously activated PCD have been found, which are divided into two categories: the first category of LLM mutants determines the initiation of PCD, such as cpr5, acd6 and ssi1, etc.
; the second category of LLMs Mutants control the strength of PCD, such as lsd1 and acd1,
etc.
The function of these proteins and the molecular mechanism of regulation between them are still unclear
.
cpr5 is an LLM mutant obtained by screening Arabidopsis cpr (constitutive expressor of pathogenesis-related genes) using the plant defense reporter gene PR2:GUS.
It has autonomously activated immunity and a phenotype similar to HR necrosis
.
RNA-seq analysis of wild-type and cpr5 mutant plants revealed that differentially expressed genes (DEGs) regulated by CPR5 overlapped 74.
9% with plant ETI-related DEGs, while only about 11.
2% overlapped with plant PTI-related DEGs, indicating that CPR5 mainly Involved in the regulation of plant ETI
.
By analyzing the CPR5 signaling pathway, three important signaling pathways were found to be involved in the regulation of plant ETI: (1) Cell cycle signaling pathway
.
The core signaling regulatory chain of the cell cycle, CKI-RB-E2F, activates plant ETI downstream of CPR5 (Wang et al.
, Cell Host & Microbe, 2014)
.
(2) Nucleocytoplasmic transport signaling pathway
.
CPR5 is a novel nucleoporin that normally forms homodimers, binds the core cell cycle regulator CKI and inhibits the nucleocytoplasmic trafficking of immune signaling molecules
.
After the plant is infected by pathogenic bacteria, the activated NLR receptor changes the conformation of CPR5, depolymerizes its dimer into monomer, releases CKI on the one hand, and opens the nuclear-cytoplasmic transport of immune signaling molecules on the other hand.
Plant ETI (Figure 1) (Dasso and Fontoura, Cell, 2016; Gu et al.
, Cell, 2016)
.
(3) RNA processing signaling pathway
.
Genetic analysis found that the RNA splicing factor NTC and the RNA poly(A) tailing factor CPSF synergistically activate plant ETI downstream of CPR5 (Peng et al.
, Plant Cell, 2022)
.
Therefore, genetic analysis of both SNC1 and CPR5 signaling reveals that plant ETI is regulated by two basic life processes, nucleocytoplasmic transport and RNA processing
.
Figure 1 After activation of the NLR receptor, the conformation of the nucleoporin CPR5 is changed.
On the one hand, it opens the nuclear pore to promote the transport of immune signaling molecules into the nucleus, and on the other hand, it releases the cell cycle core regulator CKI.
Companion PCD (adapted from Dasso and Fontoura, Cell, 2016)
.
Although most genes in the plant genome are regulated by RNA processing, such as the Arabidopsis genome, 61% of genes have RNA alternative splicing and 75% have RNA variable poly(A) tailing, so far the regulation of RNA processing Very little is known about plant immunity
.
NTC is an activator of the RNA spliceosome and consists of eight core proteins, including Prp19, CDC5L, PRL1, AD-002, SPF27, DAM1, CTNNBL1 and HSP73
.
Four of these members, Prp19, CDC5L, PRL1 and SPF27, have been found to activate plant immunity downstream of SNC1
.
In the process of plant immunity, some NLR genes undergo RNA alternative splicing, such as N gene of tobacco, RPS4 gene and SNC1 gene of Arabidopsis
.
NLR family genes may be hotspot target genes for RNA alternative splicing, the average transcript of Arabidopsis genome-wide genes is about 2.
40, while the average transcript of NLR family genes is about 3.
38
.
Some effectors of pathogenic microorganisms can directly bind to RNA splicing factors to regulate plant immunity
.
For example, HopU1 is an ADP glycosyltransferase that glycosylates two arginine residues in the RNA-binding domain RRM of GRP7 protein, blocking GRP7 from binding to the transcripts of the PRR receptors FLS2 and EFR genes on the surface of plant cells, thereby inhibiting plant growth.
PTI
.
In addition to alternative splicing, RNA variable poly(A) tailing also regulates plant immunity, particularly the CPR5 signaling pathway
.
The RNA poly(A) tailed complex contains PAPS, CPSF, CFIm, CFIIm and CSTF
.
The CPSF complex in turn contains CPSF160, CPSF100, CPSF73, CPSF30, FIP1 and WDR33
.
Arabidopsis thaliana contains 4 PAPS genes
.
PAPS1 is a negative plant immune regulator
.
Autonomously activated immune responses in paps1 mutants can be suppressed by eds1 or pad4
.
RNA-seq analysis showed that the DEGs of the paps1 mutant and the DEGs of the cpr5 mutant mostly overlapped
.
CPSF30 is a core member of the CPSF complex
.
cpsf30 mutants inhibit cell death in cpr5, lsd1 and mpk4 mutants
.
The Shui Wang team found through genetic screening that PRL1 and FIP1 activate plant immunity downstream of CPR5
.
PRL1 and FIP1 are core members of the RNA splicing factor NTC complex and the RNA poly(A) tailing factor CPSF complex, respectively
.
Further genetic analysis of other core factors of both complexes showed that both the entire NTC complex and the CPSF complex activate plant immunity downstream of CPR5
.
Analyses using BiFC-YFP, Co-IP and FRET-FLIM showed that CPR5, PRL1 and FIP1 formed a complex that co-localized in the nuclear speck of RNA-processing organelles
.
Through sequence comparison and functional substitution of different plant proteins, it was found that CPR5 is an RNA-binding protein of the Tra2 subfamily of the SR family
.
The Tra2 subfamily is a class of atypical SR family proteins with SR-RRM domains arranged in order (the RNA recognition domain RRM is arranged after the SR domain)
.
A typical SR family protein has an RRM-SR domain arrangement (RRMs are arranged before SR domains)
.
RNA-seq analysis identified 473 RNA alternatively spliced genes (ASGs) regulated by CPR5
.
AGO1 is one of these ASGs, and ago1 mutants can suppress cpr5 mutant immune responses and PCD phenotypes, suggesting that AGO1 activates plant immunity downstream of CPR5
.
Therefore, our study revealed: 1) CPR5 is an SR family RNA-binding protein; 2) The RNA splicing factor NTC and the RNA poly(A) tailing factor CPSF coordinately regulate plant immunity; 3) CPR5 links RNA processing and plant immunity Large basic life processes are linked (Figure 2)
.
Figure 2 CPR5 regulates plant immunity through the RNA splicing factor PRL1 and the RNA poly(A) tailing factor FIP1
.
(A) PRL1 (SCPR44) and FIP1 (SCPR57) activate PCD downstream of CPR5 (arrows indicate cotyledon premature senescence)
.
(B) PRL1 and FIP1 cooperatively regulate plant ETI (left) and basal immunity (right)
.
(C) BiFC-YFP analysis of CPR5, SR34, PRL1 and FIP1 subcellular colocalization
.
SR34, indicates nuclear spot location; mCherry-NLS, indicates nuclear spot location; NS, nuclear spot
.
(D) SR domain at the N-terminus of CPR5 protein, sequence comparison of different plant CPR5 proteins
.
(E) Schematic diagram of the protein structure (SR, RRM and TM domains) of the SR family Tra2 subfamily (including human RNPS1 and Arabidopsis CPR5, SR45 and SR45a proteins) (from Peng et al.
, Plant Cell, 2022)
.
In recent years, a series of studies by Wang Shui's team to analyze the regulatory pathway of CPR5 signaling revealed that CPR5, as an SR family RNA-binding protein, is the first immune signaling factor discovered so far, integrating the three basic elements of nucleocytoplasmic transport, cell cycle and RNA processing.
Life processes are integrated to regulate plant immunity (Figure 3) (Wang et al.
, Cell Host & Microbe, 2014; Gu et al.
, Cell, 2016; Peng et al.
, Plant Cell, 2022)
.
Therefore, cpr5 mutants will be an important genetic tool for dissecting ETI signaling in plants
.
Figure 3 CPR5 is an RNA-binding protein that is both a member of the nuclear pore complex (NPC) and a member of the nuclear speck
.
On the one hand, the activated NLR receptor changes the conformation of CPR5 protein, promotes the transport of immune signaling molecules into the nucleus, and releases the core cell cycle regulator CKI at the same time
.
On the other hand, CPR5 forms a complex with NTC/CPSF in the nuclear speck.
The immune signaling factors in the nucleus and CKI work together to relieve the inhibition of CPR5 on the NTC/CPSF complex, regulate RNA alternative splicing, and form transcripts encoding full-length or partial proteins.
, the ratio of the two regulates the balance between plant immunity and development
.
Peng Shun, a doctoral student from the School of Life Sciences, Shanghai Normal University, and Guo Dongbei and Guo Yuan, postgraduate students, are the co-first authors of the paper, and researcher Wang Shui is the corresponding author of the paper
.
Professor Cai Yingfan from the School of Life Sciences of Henan University and Chen Dong from Wuhan Ruixing Biotechnology Co.
, Ltd.
participated in the research of this paper
.
The research was funded by the National Natural Science Foundation of China, the Shanghai Plant Germplasm Resources Engineering Technology Research Center, and the Shanghai Key Laboratory of Plant Molecular Biology
.
Link to the original text of the Wang Shui research group (the first from the right in the second row is Wang Shui researcher): https://academic.
oup.
com/plcell/advance-article/doi/10.
1093/plcell/koac037/6524637#
