Tetrapyrrole Metabolism Is Involved in Lesion Formation, Cell Death, in the<i>Arabidopsis lesion initiation 1</i>Mutant

Ishikawa, Atsushi

doi:10.1271/bbb.69.1929

Cited by 17 publications

(10 citation statements)

References 25 publications

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“…Light dependent cell death lesions have been reported in several plant species including maize (Hu et al 1998) and A. thaliana (Laloi et al 2007). One important mechanism behind this particular phenotype is chloroplast breakdown via the tetrapyrrole metabolism (Ishikawa 2005). Since such traits are undesirable in any breeding programme, a second mutagenesis was performed and barley lines with fewer spots than the original bst1 mutant were identified.…”

Section: Resultsmentioning

confidence: 99%

Barley mutants with enhanced level of resistance to Swedish isolates of Bipolaris sorokiniana, casual agent of spot blotch

Persson¹,

Rasmussen²,

Falk³

et al. 2008

Plant Breeding

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Section: Resultsmentioning

confidence: 99%

Barley mutants with enhanced level of resistance to Swedish isolates of Bipolaris sorokiniana, casual agent of spot blotch

Persson¹,

Rasmussen²,

Falk³

et al. 2008

Plant Breeding

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“…However, GUN2-5 proteins were all found to be involved in tetrapyrrole biosynthesis; as a result, down-regulation of GUN4 via amiRNA led to reduced chlorophyll accumulation. Interestingly, Ishikawa reported that disruption of tetrapyrrole biosynthesis suppressed lesion formation in len1 , another LMM mutant [52].…”

Section: Discussionmentioning

confidence: 99%

Crosstalks between Myo-Inositol Metabolism, Programmed Cell Death and Basal Immunity in Arabidopsis

et al. 2009

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BackgroundAlthough it is a crucial cellular process required for both normal development and to face stress conditions, the control of programmed cell death in plants is not fully understood. We previously reported the isolation of ATXR5 and ATXR6, two PCNA-binding proteins that could be involved in the regulation of cell cycle or cell death. A yeast two-hybrid screen using ATXR5 as bait captured AtIPS1, an enzyme which catalyses the committed step of myo-inositol (MI) biosynthesis. atips1 mutants form spontaneous lesions on leaves, raising the possibility that MI metabolism may play a role in the control of PCD in plants. In this work, we have characterised atips1 mutants to gain insight regarding the role of MI in PCD regulation.Methodology/Principal Findings- lesion formation in atips1 mutants depends of light intensity, is due to PCD as evidenced by TUNEL labelling of nuclei, and is regulated by phytohormones such as salicylic acid - MI and galactinol are the only metabolites whose accumulation is significantly reduced in the mutant, and supplementation of the mutant with these compounds is sufficient to prevent PCD - the transcriptome profile of the mutant is extremely similar to that of lesion mimic mutants such as cpr5, or wild-type plants infected with pathogens.Conclusion/SignificanceTaken together, our results provide strong evidence for the role of MI or MI derivatives in the regulation of PCD. Interestingly, there are three isoforms of IPS in Arabidopsis, but AtIPS1 is the only one harbouring a nuclear localisation sequence, suggesting that nuclear pools of MI may play a specific role in PCD regulation and opening new research prospects regarding the role of MI in the prevention of tumorigenesis. Nevertheless, the significance of the interaction between AtIPS1 and ATXR5 remains to be established.

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“…Consistently, a mutation in the CHLOROPHYLL A/B BINDING HARVESTING-ORGANELLE SPECIFIC (CAO) gene encoding a chaperone required for the assembly photosystem II antenna leads to a reduction of lesion formation in lsd1 (Mateo et al, 2004 ). Likewise, inhibition of chlorophyll biosynthesis abolished cell death in another LMM: the mips1 mutant (Meng et al, 2009 ) and several mutations affecting chlorophyll metabolism have been reported to suppress lesion formation in len1 (Ishikawa, 2005 ). Together, these studies support the notion that perturbation of the photosynthetic metabolism can trigger PCD.…”

Section: Chloroplasts and Light Are Hubs Of Stress Leading To Pcdmentioning

confidence: 99%

To die or not to die? Lessons from lesion mimic mutants

et al. 2015

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Programmed cell death (PCD) is a ubiquitous genetically regulated process consisting in an activation of finely controlled signaling pathways that lead to cellular suicide. Although some aspects of PCD control appear evolutionary conserved between plants, animals and fungi, the extent of conservation remains controversial. Over the last decades, identification and characterization of several lesion mimic mutants (LMM) has been a powerful tool in the quest to unravel PCD pathways in plants. Thanks to progress in molecular genetics, mutations causing the phenotype of a large number of LMM and their related suppressors were mapped, and the identification of the mutated genes shed light on major pathways in the onset of plant PCD such as (i) the involvements of chloroplasts and light energy, (ii) the roles of sphingolipids and fatty acids, (iii) a signal perception at the plasma membrane that requires efficient membrane trafficking, (iv) secondary messengers such as ion fluxes and ROS and (v) the control of gene expression as the last integrator of the signaling pathways.

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Tetrapyrrole Metabolism Is Involved in Lesion Formation, Cell Death, in theArabidopsis lesion initiation 1Mutant

Cited by 17 publications

References 25 publications

Barley mutants with enhanced level of resistance to Swedish isolates of Bipolaris sorokiniana, casual agent of spot blotch

Barley mutants with enhanced level of resistance to Swedish isolates of Bipolaris sorokiniana, casual agent of spot blotch

Crosstalks between Myo-Inositol Metabolism, Programmed Cell Death and Basal Immunity in Arabidopsis

To die or not to die? Lessons from lesion mimic mutants

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