Hypersensitive response: From NLR pathogen recognition to cell death response

This study investigated the effect of CAPE on planktonic growth, biofilm-forming abilities, mature biofilms, and cell death of C. albicans, C. tropicalis, C. glabrata, and C. parapsilosis strains. Our results showed a strain- and dose-dependent effect of CAPE on Candida, and the MIC values were between 12.5 and 100 µg/mL. Similarly, the MBIC values of CAPE ranging between 50 and 100 µg/mL highlighted the inhibition of the biofilm-forming abilities in a dose-dependent manner, as well. However, CAPE showed a weak to moderate biofilm eradication ability (19-49%) on different Candida strains mature biofilms. Both caspase-dependent and caspase-independent apoptosis after CAPE treatment were observed in certain tested Candida strains. Our study has displayed typical apoptotic hallmarks of CAPE-induced chromatin margination, nuclear blebs, nuclear condensation, plasma membrane detachment, enlarged lysosomes, cytoplasm fragmentation, cell wall distortion, whole-cell shrinkage, and necrosis. In conclusion, CAPE has a concentration and strain-dependent inhibitory activity on viability, biofilm formation ability, and cell death response in the different Candida species.

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Genetic Analysis Reveals Three Novel QTLs Underpinning a Butterfly Egg-Induced Hypersensitive Response-Like Cell Death in Brassica Rapa

10.21203/rs.3.rs-1107347/v1 ◽

2021 ◽

Author(s):

Niccolò Bassetti ◽

Lotte Caarls ◽

Gabriella Bukovinszkine’Kiss ◽

Mohamed El-Soda ◽

Jeroen van Veen ◽

...

Keyword(s):

Cell Death ◽

Brassica Rapa ◽

Hypersensitive Response ◽

Genetic Basis ◽

Plant Immunity ◽

Egg Survival ◽

Crop Species ◽

Germplasm Screening ◽

Resistance To Herbivory ◽

Crop Resistance

Abstract Background Cabbage white butterflies (Pieris spp.) can be severe pests of Brassica crops such as Chinese cabbage, Pak choi (Brassica rapa) or cabbages (B. oleracea). Eggs of Pieris spp. can induce a hypersensitive response-like (HR-like) cell death which reduces egg survival in the wild black mustard (B. nigra). Unravelling the genetic basis of this egg-killing trait in Brassica crops could improve crop resistance to herbivory, reducing major crop losses and pesticides use. Here we investigated the genetic architecture of a HR-like cell death induced by P. brassicae eggs in B. rapa. Results A germplasm screening of B. rapa 56 accessions, representing the genetic and geographical diversity of a B. rapa core collection, showed phenotypic variation for cell death. An image-based phenotyping protocol was developed to accurately measure size of HR-like cell death and was then used to identify two accessions that consistently showed weak (R-o-18) or strong cell death response (L58). Screening of 160 RILs derived from these two accessions resulted in three novel QTLs for Pieris brassicae-induced cell death on chromosomes A02 (Pbc1), A03 (Pbc2), and A06 (Pbc3). The three QTLs Pbc1-3 contain cell surface receptors, intracellular receptors and other genes involved in plant immunity processes, such as ROS accumulation and cell death formation. Synteny analysis with A. thaliana suggested that Pbc1 and Pbc2 are novel QTLs associated with this trait, while Pbc3 contains also LecRK-I.1, a gene of A. thaliana previously associated with cell death induced by a P. brassicae egg extract. Conclusions This study provides the first genomic regions associated with the Pieris egg-induced HR-like cell death in a Brassica crop species. It is a step closer towards unravelling the genetic basis of an egg-killing crop resistance trait, paving the way for breeders to further fine-map and validate candidate genes.

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Hypersensitive Responses in Plants

Agricultural Reviews ◽

10.18805/ag.r-1858 ◽

2019 ◽

Cited By ~ 1

Author(s):

Ankita Thakur ◽

Shalini Verma ◽

Vedukola P Reddy ◽

Deepika Sharma

Keyword(s):

Cell Death ◽

Cell Wall ◽

Hypersensitive Response ◽

Plant Cell Wall ◽

Defense Mechanism ◽

Avirulence Gene ◽

Signal Molecules ◽

Dead Cell ◽

Natural Defense ◽

Molecular Patterns

Hypersensitivity is a natural defense for plants in response to a variety of pathogens such as viruses, bacteria, fungi and is characterized by a programmed cell death (PCD) accompanied by an accumulation of toxic compounds within the dead cell. Hypersensitive response (HR) is considered a biochemical reaction rather than a structural defense mechanism but can be seen with the naked eye or with a microscope. There are two types of hypersensitive responses: structural and induced. PCD is seen in both structural as well as in induced hypersensitive response. PCD is extreme resistance shown by the plants in which it kills its cells (suicidal death), upon a perception of the pathogen to deprive it of nutritional supply and stops its growth. Cell death plays a central role in innate immune responses in both plants and animals. Apoptosis and autophagy are physiological processes and two forms of biochemical PCD. Induced hypersensitive response comes out when the plant recognizes specific pathogen-produced signal molecules known as elicitors. Recognition of elicitors by the host plants activates an army of biochemical reactions. These reactions include an oxidative burst of reactive oxygen species (ROS), alterations in plant cell wall also including cell wall immunity (CWI) and damage-associated molecular patterns (DAMPs), induction of phytoalexins and synthesis of PR proteins. These all, are comprised under the first line of defense of plants which come into action after recognition of conserved molecules characteristic of many microbes. These are called elicitors and are known as microbeassociated or pathogen-associated molecular patterns (MAMPs or PAMPs). The second line of defense of plants is the recognition of effectors through plant resistance gene products known as R genes, which result in effector-triggered immunity (ETI). This is supported by the gene for gene hypothesis. Avirulence gene encodes a protein which is specifically recognized by genotypes of the host plant harboring the matching resistance genes.

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MMR/c-Abl-dependent activation of ING2/p73α signaling regulates the cell death response to N-methyl-N′-nitro-N-nitrosoguanidine

Experimental Cell Research ◽

10.1016/j.yexcr.2009.09.010 ◽

2009 ◽

Vol 315 (18) ◽

pp. 3163-3175 ◽

Cited By ~ 4

Author(s):

Guoming Sun ◽

Shunqian Jin ◽

R. Baskaran

Keyword(s):

Cell Death ◽

Cell Death Response

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Cadmium‐mediated toxicity in plant cells is associated with the DCD / NRP ‐mediated cell death response

Plant Cell & Environment ◽

10.1111/pce.14218 ◽

2021 ◽

Author(s):

Iana Pedro Silva Quadros ◽

Nayara Nolasco Madeira ◽

Virgílio Adriano Pereira Loriato ◽

Thaina Fernanda Fillietaz Saia ◽

Jéssica Coutinho Silva ◽

...

Keyword(s):

Cell Death ◽

Plant Cells ◽

Cell Death Response

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Estradiol-inducible AvrRps4 expression reveals distinct properties of TIR-NLR-mediated effector-triggered immunity

Journal of Experimental Botany ◽

10.1093/jxb/erz571 ◽

2020 ◽

Vol 71 (6) ◽

pp. 2186-2197 ◽

Cited By ~ 8

Author(s):

Bruno Pok Man Ngou ◽

Hee-Kyung Ahn ◽

Pingtao Ding ◽

Amey Redkar ◽

Hannah Brown ◽

...

Keyword(s):

Cell Death ◽

Cell Surface Receptor ◽

Leucine Rich Repeat ◽

Nucleotide Binding Domain ◽

Hypersensitive Cell Death ◽

Cell Death Response ◽

Defence Genes ◽

Surface Receptor ◽

Effector Triggered Immunity ◽

Bacterial Effectors

Abstract Plant nucleotide-binding domain, leucine-rich repeat receptor (NLR) proteins play important roles in recognition of pathogen-derived effectors. However, the mechanism by which plant NLRs activate immunity is still largely unknown. The paired Arabidopsis NLRs RRS1-R and RPS4, that confer recognition of bacterial effectors AvrRps4 and PopP2, are well studied, but how the RRS1/RPS4 complex activates early immediate downstream responses upon effector detection is still poorly understood. To study RRS1/RPS4 responses without the influence of cell surface receptor immune pathways, we generated an Arabidopsis line with inducible expression of the effector AvrRps4. Induction does not lead to hypersensitive cell death response (HR) but can induce electrolyte leakage, which often correlates with plant cell death. Activation of RRS1 and RPS4 without pathogens cannot activate mitogen-associated protein kinase cascades, but still activates up-regulation of defence genes, and therefore resistance against bacteria.

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