Evidence map›Paper›PMID 35277786›Full record

ArticleMolecular biology reports2022

Comparative transcriptome profiling of Polianthes tuberosa during a compatible interaction with root-knot nematode Meloidogyne incognita.

Kanchan B M Singh, Pawan Jayaswal, Shivani Chandra, Jayanthi M, Pranab Kumar Mandal

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Article in Molecular biology reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.8field-weighted citation impact, top 22% of its field
1 · What the graph read from it

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3 · Its place in the literature

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1 citing paper in PubMed, 4 citations in OpenAlex.

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4 · The record

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5 · Who and what money

Authors and funding

5 authors at 3 institutions in 1 country.

Kanchan B M SinghDivision of Nematology, ICAR- Indian Agricultural Research Institute, 110012, New Delhi, India.
Pawan JayaswalNational Institute for Plant Biotechnology, 110012, Pusa, New Delhi, India.
Shivani ChandraAmity Institute of Biotechnology, Amity University, 201313, Noida, Uttar Pradesh, India.
Jayanthi MDivision of Nematology, ICAR- Indian Agricultural Research Institute, 110012, New Delhi, India. d24551@gmail.com.
Pranab Kumar MandalNational Institute for Plant Biotechnology, 110012, Pusa, New Delhi, India. Pranabkumarmandal@gmail.com.
Amity University · INNational Research Centre on Plant Biotechnology · INIndian Agricultural Research Institute · IN

Funding

Science and Engineering Research Board EMR/2015/001647
6 · The paper itself

Abstract

backgroundThe root-knot nematode (RKN; Meloidogyne spp.) is the most destructive plant parasitic nematode known to date. RKN infections, especially those caused by Meloidogyne incognita, are one of the most serious diseases of tuberose. METHODS AND

resultsTo investigate the molecular mechanism in the host-pathogen interactions, the Illumina sequencing platform was employed to generate comparative transcriptome profiles of uninfected and Meloidogyne incognita-infected tuberose plants, during early, mid, and late infection stage. A total of 7.5 GB (49 million reads) and 9.3 GB (61 million reads) of high-quality data was generated for the control and infected samples, respectively. These reads were combined and assembled using the Trinity assembly program which clustered them into 1,25,060 unigenes. A total of 85,360 validated CDS were obtained from the combined transcriptome whereas 6,795 CDS and 7,778 CDS were found in the data for the control and infected samples, respectively. Gene ontology terms were assigned to 958 and 1,310 CDSs from the control and infected data, respectively. The KAAS pathway analysis revealed that 1,248 CDS in the control sample and 1,482 CDS in the infected sample were enriched with KEGG pathways. The major proportions of CDS were annotated for carbohydrate metabolism, signal transduction and translation related pathways in control and infected samples. Of the 8,289 CDS commonly expressed between the control and infected plants, 256 were significantly upregulated and 129 were significantly downregulated in the infected plants.

conclusionsCollectively, our results provide a comprehensive gene expression changes in tuberose during its association with RKNs and point to candidate genes that are involved in nematode stress signaling for further investigation. This is the first report addressing genes associated with M. incognita-tuberose interaction and the results have important implications for further characterization of RKN resistance genes in tuberose.

Indexed as

AsparagaceaeTylenchoideaAnimalsGene Expression ProfilingPlant DiseasesPlant RootsTranscriptomeDifferentially-expressed genesMeloidogyne incognitaNext-generation sequencingPolianthes tuberosaRoot-knot nematode

Identifiers

PMID35277786
OpenAlexW4220725873

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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.