Potential Roles for Pattern Molecule of PAMP-triggered Immunity in Improving Crop Cold Tolerance

doi:10.21203/rs.3.rs-874385/v1

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Potential Roles for Pattern Molecule of PAMP-triggered Immunity in Improving Crop Cold Tolerance

https://doi.org/10.21203/rs.3.rs-874385/v1

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published 24 Nov, 2021

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Pathogen infection cross-activates cold response and increase cold tolerance of host plants. However it is not possible to use the infection to increase cold tolerance of field plants. Here flagellin 22 (flg22), the most widely-studied PAMP, was used to mimic the pathogen infection to cross-activate cold response. Flg22 treatment alleviated the injury caused by freezing in Arabidopsis, oilseed and tobacco. In Arabidopsis, flg22 activated the expression of immunity and cold-related genes. Moreover the flg22 induced alleviation of cold injury was lost in NahG transgenic line (SA-deficient), sid2-2 and npr1-1 mutant plants, and flg22-induced expression of cold tolerance-related genes, which indicating that salicylic acid signaling pathway is required for the alleviation of cold injury by flg22 treatment. In short flg22 application can be used to enhance cold tolerance in field via a salicylic acid-depended pathway.

Plant Physiology and Morphology

Plant Molecular Biology and Genetics

freezing tolerance

flagellin 22

cross-talk

salicylic acid

The application of flagellin 22 (flg22), the most widely-studied PAMP, enhance crop cold tolerance. ICE1-CBF pathway and SA signaling is involved in the alleviation of cold injury by flg22 treatment.

Plants have worldly monitoring systems to adapt a variety of environmental disturbances including biotic and abiotic stress, such as drought, heat, cold, salinity, pathogen infection, insect feeding (Suzuki et al., 2014). Upon perceiving stress, plants trigger a series of signal transduction leading to reprogramming of gene expression to establish new balance between growth and defense response against the adverse environment to finish lifecycle and produce seeds (Zhu, 2016).

Cold stress, including chilling stress (0-15°C) and freezing stress (<0°C), restricts plant growth and development, limits plant geographical location and reduces crop production (Shi et al., 2018). C-repeat binding factors (CBFs), conserved transcription factors in many plant species, are critical for cold acclimation (Jia et al., 2016). CBF genes are rapidly induced by cold stress, and then activate the expression of downstream cold responsive gene (COR) to increase plant cold tolerance (Chinnusamy et al., 2007). CBFs are regulated by various transcription factors, which recognize the cis-elements in CBFs’ simultaneously promoters under cold stress, including ICE1 (CBF expression1), CAMTA (calmodulin-binding transcription activator) proteins, MYB15, EIN3 (Ethylene insensitive 3) (Shi et al., 2018).

Under field conditions, cold stress affects the growth and development of plants simultaneously with other stress, such as pathogen infection. Cold stress cross activates disease resistance by activating the expression of PR1, PR2, and PR5 (Pathogenesis‐Related 1, 2, and 5) through activating the function of transcription factor NAC062 (Seo et al., 2010), activating the pattern‐triggered immunity in Arabidopsis plants in a HAT1 (HISTONE ACETYL TRANSFERASE 1)‐dependent manner (Singh et al., 2014) and releasing CAMTA transcription factors mediated repression of SA biosynthesis (Kim et al., 2017). Our previous research showed that cold stress cross-activates basal immunity against bacterial pathogen Pseudomonas syringae pv tomato DC3000 (Pst DC3000) though activating SA pathway and inhibiting of JA pathway (Wu et al., 2019). Interestingly this pathogen infection also cross-activates cold response and thus increase cold tolerance of host plants (Tuang et al., 2020). These investigations provide an idea to exploit immunity to increase plants abiotic stress tolerance.

Plants has a multilayered system to defense against pathogens, plant cells are able to recognize conserved epitopes of pathogen, which called pathogen-associated molecular patterns (PAMPs), such as bacterial flagellin (Wyrsch et al., 2015). Plasma membrane-localized pattern recognition receptors (PRRs) activates PAMP-triggered immunity (PTI), a mild and wide-spectrum disease resistance against various pathogens (Bigeard et al., 2015). Flagellin-22 (Flg22), the most widely-studied PAMP, has a conserved 22-amino acid domain shared by the bacterial flagellum. Flg22 is recognized by flagellin sensing 2 (FLS2) and activates a mitogen-activated protein kinase (MAPK) cascade that regulates the activation of defense-related genes (Zipfel et al., 2004), including salicylic acid (SA) pathway maker genes such as PR1, PAD4, EDS1, NPR1 (Denoux et al., 2009), callose deposition (Muthamilarasan & Prasad, 2013), and production of reactive oxygen species (ROS) (Bigeard et al., 2015).

In this work, it is investigated whether flg22, a well-studied PAMP is able to cross-activate cold response and thus increase the cold tolerance of plants and our data indicated that the PAMP is a potential activator useful for improve the cold tolerance of crops.

Flg22 treatment alleviated the injury caused by freezing in Arabidopsis

In previous work, it was shown that bacterial pathogen Pst DC3000 infection cross-activates the cold response and thus increased cellular viability under freezing (Tuang et al., 2020). As the pathogen infection leads to serious disease to plants, it is not possible to use the infection to increase freezing tolerance of field plants. Thus we investigated whether flg22, (a pathogen associated molecular patterns PAMPs), a maker peptide for PTI in freezing stress response, derived from bacterial flagellin proteins, could mimic the pathogen infection to cross-activate cold response to some extent.

Five days old Arabidopsis seedlings were treated with flg22, and 2 days later the infiltrated (2 dpi) seedlings were stressed under -4°C for 1 h, 2 h, and 2.5 h respectively. Then extracted the chlorophyll and determine the contents using UV-Spectrometer. As shown in Figure 1, both chlorophyll ‘a’ and ‘b’ of flg22 treated seedlings showed lower chlorophyll contents compared to control seedlings under control condition (22°C). However, at 1 h freezing stress, chlorophyll ‘a’ & ‘b’ in control and flg22 treated seedlings showed no difference. At 2 h freezing stressed flg22 treated seedlings showed higher contents compared to those of control seedlings (Figure 1). The results indicated that freezing stress not much effect chlorophyll contents in a test temperature and time points, but prior flg22 treatment induced chlorophyll contents upon freezing stress in Arabidopsis seedlings.

To further examine whether Flg22 treatment functions as pathogen infection under freezing stress. Arabidopsis plants were infiltrated by flg22, and 2 days later the infiltrated plants were stressed under freezing temperature (-4°C) for 6 h or 8 h, and the cellular viability was evaluated by trypan blue staining and ion leakage measurement. As shown in Figure 2, upon freezing, the CK (non-infiltrated), Mock (infiltrated by water), and flg22-infiltrated plants were significantly decreased in cellular viability and increased ion leakage level compared with their counterpart controls (non-freezing) (Figure 2). However, after 8 h of freezing stress, flg22-infiltrated plants showed significant higher cellular viability and lower ion leakage level than CK and mock plants (Figure2a & c). These results indicate that prior flg22 treatment could alleviate cellular injury caused by subsequent freezing stress.

Flg22 infiltration induced chlorophyll contents of Oilseed and Tobacco seedlings upon freezing

To know whether flg22 treatment affects freezing tolerance in crops as found in Arabidopsis, we also treated five days old Brassica napus (winter Oilseed Rape) seedlings by flg22, and 2 dpi seedlings were stressed under -4°C. As shown in Figure 3 chlorophyll ‘a’ of flg22 treated seedlings showed higher contents than those of control seedlings in 1 h, 2 h, and 2.5 h of freezing stressed (Figure 3); and chlorophyll ‘b’ of flg22 treated seedlings showed higher contents than those of control seedlings in 2 h, and 2.5 h of freezing stressed (Figure3). This result suggests that prior flg22 treatment-induced chlorophyll contents upon freezing stress.

Then we checked the chlorophyll contents of Nicotiana tabacum (Tobacco) seedlings upon freezing stress. Similar to Oilseed, Tobacco seedlings also showed higher chlorophyll contents in flg22 treated seedlings (Figure 4) compared to control seedlings upon freezing stress. Under normal conditions (22°C), control and flg22 treated seedlings showed no significant contents to each other. However, chlorophyll contents of flg22 prior treated seedlings showed higher contents compared to control seedlings after freezing stress (Figure 4). All chlorophyll contents were down to basal level at 2.5 h of freezing stress (Figure 3, 2.5 h). The results suggest freezing stress adversely affects the chlorophyll contents of Tobacco, and flg22 treatment indeed induced chlorophyll contents upon freezing stress in tested conditions. All these above indicates that flg22 treatment enhanced freezing tolerance in oilseed and tobacco.

Flg22 treatment activated the expression of cold-related genes

As higher cellular viability was detected in flg22-treated plants stressed by freezing (Figure 4a-4b) and our previous work showed the pathogen infection activated the expression of cold-responsive genes in host plants (Tuang et al, 2020), it was asked whether flg22 treatment also cross-induces these genes expression. We checked the expressions of some cold stress-related genes. As expected, some key genes involved in cold tolerance were activated by flg22 at early (6 hpi) or/and late (48 hpi) stages. Interestingly, some of tested genes were only upregulated at early stage, including ICE1, CBF3, COR15A (Figure 5a, d and e). CBF1, COR15B, COR27 and COR413M2 were upregulated at both early and late stages (Figure 5b, f, g and h).

To find out the genetic mechanism on flg22 treatment increasing cold tolerance, we analyzed the expression of more genes which play positive function in cold tolerance. The expression of CHS1, ATERDJ3A, DREB2A, MBF1C (Figure 6a, c, g and i).were induced at both early and late stages. The expression of AZI1, MKK2, DREB2C, EARLI1, NAC019, NAC042 (Figure 6b, f, h, i, j and k).were only upregulated at early stage. The expression of flg22-activated immunity genes such as EDS1, EDS5, EDS16 and PR1 which were upregulated at both early and late stages (Supplement Figure 1). All these results indicate flg22 treatment, similar to pathogen injection, activates the expression of genes involved cold response pathway in host plants.

Flg22-activated cold tolerance is dependent on SA

Salicylic acid (SA) is required for the alleviation of cold injury by pst Dc3000, therefore we wondered whether the alleviation of cold injury by Flg22 was associated with SA accumulation. NahG transgenic plant, containing a salicylate hydroxylase gene NahG, was an SA deficient line (Tuang et al., 2020). As shown in figure 7a & c under freezing for 6 hours flg22 treated NahG plants showed no difference in cell viability and ion leakage with control and mock treated plants. After -4°C treatment for 8 hours flg22 infected NahG plants were more severely damaged by freezing than CK and mock ones (figure 7a&c), which was contrast with the results detected in wildtype. NahG transgenic plant, SA deficient line, lost the capacity of alleviating freezing injury by flg22 treatment, indicating SA was required in the alleviating.

To confirm the function of SA in alleviation of cold injury by flg22 treatment, the cold tolerance of flg22 treated sid2-2 and npr1-1 plants was checked. SID2 plays an important role in SA accumulation, pathogen induced SA biosynthesis was significantly decreased in sid2-2 mutant plants (Dempsey et al., 2011). The SA induced by pathogen induce the expression of downstream genes by activate NPR1 (Pajerowska-Mukhtar et al., 2013). NPR1 is the regulator of SA signaling pathway. As shown in figure 7e-l, flg22 treated sid2-2 and npr1-1 plants showed no difference in cell viability and ion leakage with control and mock treated plants under freezing for 6 hours. Flg22 treated sid2-2 plants were more severely damaged by freezing for 8 hours than CK and mock ones. These above indicated the requirement of SID and NPR for the alleviation of freezing injury by flg22 treatment.

The effect of flg22 treatment on expression of cold tolerance genes was lost or compromised in NahG, sid2-2, and npr1-1 plants

To check whether SA was required for the activation of genes which were related the cold tolerance and induced by flg22 treatment, the expression of these genes were detected in flg22 treated NahG transgenic, sid2-2, npr1-1 plants. As shown in figure 8 the induction by flg22 infection of genes, including CBF1, CBF3, ATERDJ3A, NAC042, was lost in NahG transgenic plants. Only the expression of DREB2C and MBF1C was partially induced. In sid2-2 mutant plants the induction of CBF1, CBF3, DREB2C, MBF1C was completely lost (figure 8). In npr1-1 mutant plants the induction of CBF1, CBF3, DREB2C, NAC042 and MBF1C was completely lost (figure 8). All these above indicated that NPR1-mediated SA signaling pathway is required for the activation of these cold tolerance related genes.

Flagellin-22 treatment alleviates the injury caused by subsequent freezing stress

A great deal of evidences showed the crosstalk between abiotic stress and immune response, environmental factors are proved to modulate plant immunity (Saijo and Loo, 2020). For example, UV-B or excessive light stress induced the synthetize of flavonoids (Schenke et al., 2019), which weaken SA-based immunity (Serrano et al., 2012); heat stress induced the expression of HSP, which enhanced plant immunity by the accumulation and stability of pathogenesis-related (PR) proteins (Ul Haq et al., 2019); cold stress activated disease resistance through SA dependent pathway (Wu et al., 2019). Our earlier experiment showed that pst DC3000 infection enhanced the tolerance of freezing and heat injury in Arabidopsis (Tuang et al., 2020). However these findings are not possible for use in field because lack of practicability or the damage to plants.

Here, flagellin-22 treatment not only alleviated freezing injury in Arabidopsis (Figure 1&2) but also in oilseed (Figure 3) and tobacco (Figure 4). Flg22, a conserved peptide with 22 amino acid, has been widely used to induce PTI responses and does not lead to serious disease to plant (Wyrsch et al., 2015). All these above suggested that flg22 application may be used to enhance cold tolerance in field.

Flagellin-22 treatment activates signaling pathway of cold stress

When exposed to cold stress, plant rapidly induces the expression of many transcription factors, including the APETALLA2 (AP2)-domain proteins CBFs (CBF1, CBF2 and CBF3). The expression of CBF genes was regulated by ICE1, a bHLH transcription factor (Chinnusamy et al., 2007). In Arabidopsis, CBF2 is suggested as a negative regulator of CBF1 and CBF3 expression during cold response (Novillo et al., 2004). The cold-induced CBFs bind C-repeat/ dehydration-responsive elements in the promoters of downstream genes and activate the expression of downstream genes, such as numerous COR genes (Zhu 2016).Interestingly, in our work, the expression of ICE1 was induced by flg22 treatment at early stage (6 hours after injection), the expression of CBF1 and CBF3 was up-regulated by flg22 and the expression of CBF2 was depressed by flg22 treatment at early and late stages (Figure 5). Furthermore a sum of COR genes were up-regulated by flg22 treatment, including COR15A, COR15B, COR27, COR143M2 (Figure 5). These results suggested that the ICE1-CBF pathway is activated by flg22, thus increasing cold tolerance of host plants.

SA is required for alleviating the injury caused by cold stress

Salicylic acid (SA) has emerged as a key plant defense hormone for both pathogen-associated molecular patterns (PAMPs)-triggered immunity (PTI) and effector-triggered immunity (ETI) (Zhang and Li, 2019). SA also plays an important role in the plant responses to different abiotic stresses (Rivas-San and Plasencia, 2011). Cold was shown to induce SA biosynthesis (Kim et al., 2013 & 2017), meanwhile exogenous SA treatment was proved to provide protection against cold stress (Miura & Furumoto, 2013). Flg22 treatments caused SA accumulation through SID2-mediated SA biosynthesis (Tsuda et al., 2008). SID2, which encodes isochorismate synthase, is a SA biosynthetic enzyme (Wildermuth et al., 2001).

Our current work showed Flg22 treatment induced SA was required for the alleviation of subsequent cold injury, since both NahG line and sid2-2 mutant plants lost the ability to alleviating the injury (Figure 7). Consistently, in these plants, Flg22 treatment-activated expression of tested cold stress genes was lost or compromised (Figure 8). Moreover, the alleviation of cold injury by Flg22 was lost in npr1-1 mutant (Figure 7 & 8), which suggest SA signaling pathway also play a vital role in flg22 enhanced cold tolerance.

In summary, our work suggested that flg22 application may be used to enhance cold tolerance in field, indicated that flg22 treatment enhance of host plants to cold stress by activating cold signaling pathway ICE1-CBF. NPR1-mediated SA signaling is involved in the alleviation of cold injury by prior flg22 treatment.

Plant materials and flg22 treatment

The Arabidopsis materials including ecotype Col-0, npr1-1 and sid2-1, NahG transgenic plants and growth conditions were described in Tuang et al (2020). The four-week-old plants with the 8^th true leaf emerging were vacuum-infiltrated by 2 mg/L of Flg22 at -0.1 MPa for 1 min, followed by culturing under the normal condition for 2 days. Then, the plants were moved to -4℃ for different time. The cellular viability, Chlorophyll contents and ion leakage were measured upon each time-point. Freezing treatment were performed under a dark condition.

For oilseed and tobacco materials, seeds were sown on half MS basal agar plates, and cold acclimated at 4°C for 48 h, then transferred to 22-23°C for germination. 5-day-old seedlings on growing plates were sprayed by 2 mg/L flg22 solution, and sequentially cultured for 2 days. Then plates were moved to -4℃ incubator for 1 h, 2 h, 2.5 h, and the chlorophyll contents were measured upon each time-point for evaluating the freezing damage.

Cellular viability assay and Chlorophyll contents measurement

Electrical conductance and trypan blue staining were used to evaluate the cellular viability as described in Tuang et al., (2020). Chlorophyll extraction was performed by following the method from Karan & Subudhi, (2012).

RNA isolation and Real-Time PCR

Total RNAs were extracted from Arabidopsis leaves with NucleoZol solution (Macherey-Nagel GmbH & Co. KG, Germany) following the manufacturer’s instructions. Prime Script™ RT Reagent Kit with gDNA Eraser (Takara Bio Inc. China) was used to remove DNA contamination and synthesize cDNA. All qPCR reactions were performed using the UNICON^TMSYBR^® Green master mix (Yeasen Co. Ltd, China). TUB2 (At5g62690) was used as the internal control. The data were shown as the average ± SD from three biological replicates. Primers were described in our previous work (Tuang et al., 2020).

Statistics

The statistics analysis was performed using the software GraphPad Prism (Version 7.00). Student’s t was used to test the significance of a single pair of sample differences. One-way ANOVA analysis of variance was used to test the significance of the differences between multiple pairs of samples, with Tukey's multiple comparisons test for a post-hoc test for pairwise significant comparison. A difference at P < 0.05 was considered significant.

Author Contribution

YJ and WY conceived and designed research. ZT ,YJ, YW and ZW conducted experiments. YJ wrote the manuscript. All authors read and approved the manuscript.

Conflict of interest

The authors declare that they have no conflict of interest.

Funding

This work was financially supported by the National Natural Science Foundation of China (grant numbers 31470365 and 31700216)

Data availability

All data generated or analysed during this study are included in this published article and its supplementary information files.

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You are reading this latest preprint version

Potential Roles for Pattern Molecule of PAMP-triggered Immunity in Improving Crop Cold Tolerance

Status:

Journal Publication

Version 1

Abstract

Figures

Key message

Introduction

Results

Flg22 treatment alleviated the injury caused by freezing in Arabidopsis

Flg22 infiltration induced chlorophyll contents of Oilseed and Tobacco seedlings upon freezing

Flg22 treatment activated the expression of cold-related genes

Flg22-activated cold tolerance is dependent on SA

The effect of flg22 treatment on expression of cold tolerance genes was lost or compromised in NahG, sid2-2, and npr1-1 plants

Discussion

Flagellin-22 treatment alleviates the injury caused by subsequent freezing stress

Flagellin-22 treatment activates signaling pathway of cold stress

SA is required for alleviating the injury caused by cold stress

Materials And Methods

Plant materials and flg22 treatment

Cellular viability assay and Chlorophyll contents measurement

RNA isolation and Real-Time PCR

Statistics

Declarations

Author Contribution

Conflict of interest

Funding

Data availability

References

Supplementary Files

Status:

Journal Publication

Version 1