Evidence map›Paper›PMID 28508261›Full record

ReviewPlanta2017

Functional roles of the pepper leucine-rich repeat protein and its interactions with pathogenesis-related and hypersensitive-induced proteins in plant cell death and immunity.

Jeum Kyu Hong, In Sun Hwang, Byung Kook Hwang

Abstract readReview
PubMed Publisher
In one paragraph

Review in Planta, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
11.2field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

10 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Silencing a Simple Extracellular Leucine-Rich Repeat GeneInternational journal of molecular sciences · 2021
    Article
  5. Article
  6. Article
  7. CRISPR/Cas9-mediatedHorticulture research · 2020
    Article
  8. Article
  9. Article
  10. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 3 institutions in 1 country.

Jeum Kyu HongLaboratory of Plant Pathology and Protection, Department of Horticultural Science, College of Biosciences, Gyeongnam National University of Science and Technology, Jinju, 52725, Republic of Korea.
In Sun HwangDepartment of Horticultural Biotechnology, Kyung Hee University, Yongin, 17104, Republic of Korea.
Byung Kook HwangLaboratory of Molecular Plant Pathology, College of Life Sciences and Biotechnology, Korea University, Seoul, 02841, Republic of Korea. bkhwang@korea.ac.kr.ORCID http://orcid.org/0000-0003-1782-8990
Gyeongnam National University of Science and Technology · KRKorea University · KRKyung Hee University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MAIN

conclusionPepper leucine-rich repeat protein (CaLRR1) interacts with defense response proteins to regulate plant cell death and immunity. This review highlights the current understanding of the molecular functions of CaLRR1 and its interactor proteins. Plant cell death and immune responses to microbial pathogens are controlled by complex and tightly regulated molecular signaling networks. Xanthomonas campestris pv. vesicatoria (Xcv)-inducible pepper (Capsicum annuum) leucine-rich repeat protein 1 (CaLRR1) serves as a molecular marker for plant cell death and immunity signaling. In this review, we discuss recent advances in elucidating the functional roles of CaLRR1 and its interacting plant proteins, and understanding how they are involved in the cell death and defense responses. CaLRR1 physically interacts with pepper pathogenesis-related proteins (CaPR10 and CaPR4b) and hypersensitive-induced reaction protein (CaHIR1) to regulate plant cell death and defense responses. CaLRR1 is produced in the cytoplasm and trafficked to the extracellular matrix. CaLRR1 binds to CaPR10 in the cytoplasm and CaPR4b and CaHIR1 at the plasma membrane. CaLRR1 synergistically accelerates CaPR10-triggered hypersensitive cell death, but negatively regulates CaPR4b- and CaHIR1-triggered cell death. CaHIR1 interacts with Xcv filamentous hemagglutinin (Fha1) to trigger disease-associated cell death. The subcellular localization and cellular function of these CaLRR1 interactors during plant cell death and defense responses were elucidated by Agrobacterium-mediated transient expression, virus-induced gene silencing, and transgenic overexpression studies. CaPR10, CaPR4b, and CaHIR1 positively regulate defense signaling mediated by salicylic acid and reactive oxygen species, thereby activating hypersensitive cell death and disease resistance. A comprehensive understanding of the molecular functions of CaLRR1 and its interacting protein partners in cell death and defense responses will provide valuable information for the molecular genetics of plant disease resistance, which could be exploited as a sustainable disease management strategy.

Indexed as

CapsicumCell DeathLeucine-Rich Repeat ProteinsPlant DiseasesPlant ImmunityPlant ProteinsProteinsLeucine-Rich Repeat ProteinsPlant ProteinsProteinsCell deathDefense responseLeucine-rich repeat (LRR) proteinPathogenesis-related (PR) proteinPepper (Capsicum annuum)Protein–protein interaction

Identifiers

PMID28508261
OpenAlexW2614966187

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.