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

Author(s):  
Niccolò Bassetti ◽  
Lotte Caarls ◽  
Gabriella Bukovinszkine’Kiss ◽  
Mohamed El-Soda ◽  
Jeroen van Veen ◽  
...  

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.

2021 ◽  
Author(s):  
Tongbing Su ◽  
Weihong Wang ◽  
Peirong Li ◽  
Xiaoyun Xin ◽  
Yangjun Yu ◽  
...  

2018 ◽  
Vol 11 (11) ◽  
pp. 1360-1376 ◽  
Author(s):  
Tongbing Su ◽  
Weihong Wang ◽  
Peirong Li ◽  
Bin Zhang ◽  
Pan Li ◽  
...  

2016 ◽  
Vol 80 (4) ◽  
pp. 748-760 ◽  
Author(s):  
Yuka Ootsubo ◽  
Takanori Hibino ◽  
Takahito Wakazono ◽  
Yukio Mukai ◽  
Fang-Sik Che

Author(s):  
Ankita Thakur ◽  
Shalini Verma ◽  
Vedukola P Reddy ◽  
Deepika Sharma

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.


2011 ◽  
Vol 24 (1) ◽  
pp. 68-78 ◽  
Author(s):  
Hyong Woo Choi ◽  
Young Jin Kim ◽  
Byung Kook Hwang

Pathogen-induced programmed cell death (PCD) is intimately linked with disease resistance and susceptibility. However, the molecular components regulating PCD, including hypersensitive and susceptible cell death, are largely unknown in plants. In this study, we show that pathogen-induced Capsicum annuum hypersensitive induced reaction 1 (CaHIR1) and leucine-rich repeat 1 (CaLRR1) function as distinct plant PCD regulators in pepper plants during Xanthomonas campestris pv. vesicatoria infection. Confocal microscopy and protein gel blot analyses revealed that CaLRR1 and CaHIR1 localize to the extracellular matrix and plasma membrane (PM), respectively. Bimolecular fluorescent complementation and coimmunoprecipitation assays showed that the extracellular CaLRR1 specifically binds to the PM-located CaHIR1 in pepper leaves. Overexpression of CaHIR1 triggered pathogen-independent cell death in pepper and Nicotiana benthamiana plants but not in yeast cells. Virus-induced gene silencing (VIGS) of CaLRR1 and CaHIR1 distinctly strengthened and compromised hypersensitive and susceptible cell death in pepper plants, respectively. Endogenous salicylic acid levels and pathogenesis-related gene transcripts were elevated in CaHIR1-silenced plants. VIGS of NbLRR1 and NbHIR1, the N. benthamiana orthologs of CaLRR1 and CaHIR1, regulated Bax- and avrPto-/Pto-induced PCD. Taken together, these results suggest that leucine-rich repeat and hypersensitive induced reaction proteins may act as cell-death regulators associated with plant immunity and disease.


2018 ◽  
Vol 31 (10) ◽  
pp. 1006-1020 ◽  
Author(s):  
Huwei Hou ◽  
Ya Hu ◽  
Qian Wang ◽  
Xiongbiao Xu ◽  
Yajuan Qian ◽  
...  

In this study, we used high-throughput deep nucleotide sequencing to characterize the global transcriptional response of Nicotiana benthamiana plants to transient expression of the RepA protein from Oat dwarf virus (ODV). We identified 7,878 significantly differentially expressed genes (DEG) that mapped to 125 pathways, suggesting that comprehensive networks are involved in regulation of RepA-induced cell death. Of the 202 DEG associated with photosynthesis, expression of 195 was found to be downregulated, indicating a significant inhibition of photosynthesis in response to RepA expression, which is associated with chloroplast disruption and physiological changes. We focused our analysis on NbFDN1, a member of the ferredoxin protein family that participates in the chloroplast electron transport chain performing oxygenic photosynthesis, which was identified to directly interact with NbTsip1. We separately knocked down the expression of NbFDN1 and NbTsip1 using virus-induced gene silencing, and found that NbFDN1 silencing speeded up the development of RepA-induced cell death, unlike NbTsip1 silencing, which showed an opposite effect on RepA-induced response. Further study showed increased H2O2 accumulation and a negative correlation between the transcripts of NbFDN1 and NbTsip1 in NbFDN1-silenced plants. Hence, we speculate that NbFDN1 has an effect on RepA-induced hypersensitive response-like response by modulating NbTsip1 transcription as well as H2O2 production.


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