Evidence map›Paper›PMID 38427069›Full record

ArticlePlanta2024

Mutation in Arabidopsis mitochondrial Pentatricopeptide repeat 40 gene affects tolerance to water deficit.

Kamal Kant, Gábor Rigó, Dóra Faragó, Dániel Benyó, Roland Tengölics, László Szabados, Laura Zsigmond

Erratum issuedOpen access · hybridAbstract read
In one paragraph

Article in Planta, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

3 citing papers in PubMed, 4 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Kamal KantInstitute of Plant Biology, HUN-REN Biological Research Centre, Temesvári Krt. 62, 6726, Szeged, Hungary.
Gábor RigóInstitute of Plant Biology, HUN-REN Biological Research Centre, Temesvári Krt. 62, 6726, Szeged, Hungary.
Dóra FaragóInstitute of Plant Biology, HUN-REN Biological Research Centre, Temesvári Krt. 62, 6726, Szeged, Hungary.
Dániel BenyóInstitute of Plant Biology, HUN-REN Biological Research Centre, Temesvári Krt. 62, 6726, Szeged, Hungary.
Roland TengölicsInstitute of Biochemistry, HUN-REN Biological Research Centre, Temesvári Krt. 62, 6726, Szeged, Hungary.
László Szabados *Institute of Plant Biology, HUN-REN Biological Research Centre, Temesvári Krt. 62, 6726, Szeged, Hungary. szabados.laszlo@brc.hu.ORCID http://orcid.org/0000-0002-9163-9875
Laura Zsigmond *Institute of Plant Biology, HUN-REN Biological Research Centre, Temesvári Krt. 62, 6726, Szeged, Hungary.
HUN-REN Szegedi Biológiai Kutatóközpont · HU

Funding

Nemzeti Kutatási Fejlesztési és Innovációs Hivatal FK128920Nemzeti Kutatási Fejlesztési és Innovációs Hivatal GINOP-2.3.3-15-2016-00023Nemzeti Kutatási Fejlesztési és Innovációs Hivatal K128728Nemzeti Kutatási Fejlesztési és Innovációs Hivatal K143620
6 · The paper itself

Abstract

MAIN

conclusionThe Arabidopsis Pentatricopeptide repeat 40 (PPR40) insertion mutants have increased tolerance to water deficit compared to wild-type plants. Tolerance is likely the consequence of ABA hypersensitivity of the mutants. Plant growth and development depend on multiple environmental factors whose alterations can disrupt plant homeostasis and trigger complex molecular and physiological responses. Water deficit is one of the factors which can seriously restrict plant growth and viability. Mitochondria play an important role in cellular metabolism, energy production, and redox homeostasis. During drought and salinity stress, mitochondrial dysfunction can lead to ROS overproduction and oxidative stress, affecting plant growth and survival. Alternative oxidases (AOXs) and stabilization of mitochondrial electron transport chain help mitigate ROS damage. The mitochondrial Pentatricopeptide repeat 40 (PPR40) protein was implicated in stress regulation as ppr40 mutants were found to be hypersensitive to ABA and high salinity during germination. This study investigated the tolerance of the knockout ppr40-1 and knockdown ppr40-2 mutants to water deprivation. Our results show that these mutants display an enhanced tolerance to water deficit. The mutants had higher relative water content, reduced level of oxidative damage, and better photosynthetic parameters in water-limited conditions compared to wild-type plants. ppr40 mutants had considerable differences in metabolic profiles and expression of a number of stress-related genes, suggesting important metabolic reprogramming. Tolerance to water deficit was also manifested in higher survival rates and alleviated growth reduction when watering was suspended. Enhanced sensitivity to ABA and fast stomata closure was suggested to lead to improved capacity for water conservation in such environment. Overall, this study highlights the importance of mitochondrial functions and in particular PPR40 in plant responses to abiotic stress, particularly drought.

Indexed as

ArabidopsisArabidopsis ProteinsAbscisic AcidDroughtsGene Expression Regulation, PlantMutationPlants, Genetically ModifiedReactive Oxygen SpeciesStress, PhysiologicalWaterAbscisic AcidArabidopsis ProteinsReactive Oxygen SpeciesWaterArabidopsisDrought toleranceMitochondriaMutant analysisOxidative stressPentatricopeptide repeat 40Water deficit

Identifiers

PMID38427069
PMCPMC10907415
OpenAlexW4392385689

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.