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To Die or Not to Die? Lessons From Lesion Mimic Mutants


To Die or Not to Die? Lessons From Lesion Mimic Mutants

Quentin Bruggeman et al. Front Plant Sci.


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.

Keywords: genetics approaches; immunity responses; lesion mimic mutants; plant; programmed cell death.


Figure 1
Figure 1
Simplified representation of the tetrapyrrole biosynthesis pathway and chlorophyll catabolism into the chloroplast. Factors disrupted in LMM are indicated in red whereas factor disrupted in suppressors of LMM are in green. ACD1/PAO1/LLS1, Accelerated cell death 1/Pheophorbide a oxygenase/Lethal leaf spot1; ACD2/RCCR, Accelerated cell death 2/Red chlorophyll catabolite reductase; ChlS, Chlorophyll synthase; FC, Fe chelatase; FLU, Fluorescent; GLU-TR, Glutamyl-tRNA reductase; LES22/UROD, Lesion 22/Uroporphyrinogen III decarboxylase; LIN2/CPO, Lesion initiation 2/Coproporphyrinogen III oxidase; Mg-Ch, Mg chelatase; OEP16-1, Outer plastid envelope protein 16-1; PBS, Phytochromobilin synthase; PORA, NADPH-protochlorophyllide oxidoreductase; PPO, Protoporphyrinogen IX oxidase; RUG1/PGBD, Rugosa 1/Porphobilinogen deaminase; ULF3/HY1, FLU3 written backwards/Heme oxygenase 1; UPM, Uroporphyrinogen III methylase; UROS, Uroporphyrinogen III synthase.
Figure 2
Figure 2
Simplified representation of sphingolipid metabolism in plants. The de novo biosynthesis of ceramides occurs in the endoplasmic reticulum and synthesis of more complex sphingolipids occurs in the Golgi. Sphingosine and phytosphingosine are both referred in the text as Long-chain Basis (LCB). Factors disrupted in LMM are indicated in red. AAL, Alternaria alternata f. sp. lycopersici; ACD5/11, Accelerated cell death 5/11, are a ceramide kinase and a ceramide-1-phosphate transporter, respectively; ERH1/IPCS2, Enhancing RPW8-mediated HR-like cell death 1/Inositolphosphoceramide synthase 2; FB1, Fumosin B1; LCB1/2a/2b, Long-chain base 1/2a/2b, are subunits which form the Serine palmitol-transferase; LOH1/2/2 Lag one homolog1/2/3, are ceramide synthases; MIPS1, Myo-inositol-1-phosphate synthase; PIS, Phosphatidylinositol synthase; SBH, Sphingoid base hydroxylase; SphK, Sphingosin kinase.

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