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.

Programmed cell death (PCD) is essential for several aspects of plant life, including development and stress responses. Indeed, incompatible plant-pathogen interactions are well known to induce the hypersensitive response, a localized cell death. Mutational analyses have identified several key PCD components, and we recently identified the mips1 mutant of Arabidopsis (Arabidopsis thaliana), which is deficient for the key enzyme catalyzing the limiting step of myoinositol synthesis. One of the most striking features of mips1 is the light-dependent formation of lesions on leaves due to salicylic acid (SA)-dependent PCD, revealing roles for myoinositol or inositol derivatives in the regulation of PCD. Here, we identified a regulator of plant PCD by screening for mutants that display transcriptomic profiles opposing that of the mips1 mutant. Our screen identified the oxt6 mutant, which has been described previously as being tolerant to oxidative stress. In the oxt6 mutant, a transfer DNA is inserted in the CLEAVAGE AND POLYADENYLATION SPECIFICITY FACTOR30 (CPSF30) gene, which encodes a polyadenylation factor subunit homolog. We show that CPSF30 is required for lesion formation in mips1 via SA-dependent signaling, that the prodeath function of CPSF30 is not mediated by changes in the glutathione status, and that CPSF30 activity is required for Pseudomonas syringae resistance. We also show that the oxt6 mutation suppresses cell death in other lesion-mimic mutants, including lesion-simulating disease1, mitogen-activated protein kinase4, constitutive expressor of pathogenesis-related genes5, and catalase2, suggesting that CPSF30 and, thus, the control of messenger RNA 39 end processing, through the regulation of SA production, is a key component of plant immune responses.

Programmed cell death (PCD) is essential for several aspects of plant life, including development and stress responses. We recently identified the mips1 mutant of Arabidopsis thaliana, which is deficient for the enzyme catalyzing the limiting step of myo-inositol (MI) synthesis. One of the most striking features of mips1 is the light-dependent formation of lesions on leaves due to salicylic acid (SA)-dependent PCD. Here, we identified a suppressor of PCD by screening for mutations that abolish the mips1 cell death phenotype. Our screen identified the hxk1 mutant, mutated in the gene encoding the hexokinase1 (HXK1) enzyme that catalyzes sugar phosphorylation and acts as a genuine glucose sensor. We show that HXK1 is required for lesion formation in mips1 due to alterations in MI content, via SA-dependant signaling. Using two catalytically inactive HXK1 mutants, we also show that hexokinase catalytic activity is necessary for the establishment of lesions in mips1. Gas chromatography-mass spectrometry analyses revealed a restoration of the MI content in mips1 hxk1 that it is due to the activity of the MIPS2 isoform, while MIPS3 is not involved. Our work defines a pathway of HXK1-mediated cell death in plants and demonstrates that two MIPS enzymes act cooperatively under a particular metabolic status, highlighting a novel checkpoint of MI homeostasis in plants.

The cell cycle is one of the most comprehensively studied biological processes, due primarily to its significance in growth and development, and its deregulation in many human disorders. Studies using a diverse set of model organisms, including yeast, worms, flies, frogs, mammals, and plants, have greatly expanded our knowledge of the cell cycle and have contributed to the universally accepted view of how the basic cell cycle machinery is regulated. In addition to the oscillating activity of various cyclin-dependent kinase (CDK)-cyclin complexes, a plethora of proteins affecting various aspects of chromatin dynamics has been shown to be essential for cell proliferation during plant development. Furthermore, it was reported recently that core cell cycle regulators control gene expression by modifying histone patterns. This review focuses on the intimate relationship between the cell cycle and chromatin. It describes the dynamics and functions of chromatin structures throughout cell cycle progression and discusses the role of heterochromatin as a barrier against re-replication and endoreduplication. It also proposes that core plant cell cycle regulators control gene expression in a manner similar to that described in mammals. At present, our challenge in plants is to define the complete set of effectors and actors that coordinate cell cycle progression and chromatin structure and to understand better the functional interplay between these two processes.

Programmed cell death (PCD) is a crucial process both for plant development and responses to biotic and abiotic stress. There is accumulating evidence that chloroplasts may play a central role during plant PCD as for mitochondria in animal cells, but it is still unclear whether they participate in PCD onset, execution, or both. To tackle this question, we have analyzed the contribution of chloroplast function to the cell death phenotype of the myoinositol phosphate synthase1 (mips1) mutant that forms spontaneous lesions in a light-dependent manner. We show that photosynthetically active chloroplasts are required for PCD to occur in mips1, but this process is independent of the redox state of the chloroplast. Systematic genetic analyses with retrograde signaling mutants reveal that 39-phosphoadenosine 59-phosphate, a chloroplast retrograde signal that modulates nuclear gene expression in response to stress, can inhibit cell death and compromises plant innate immunity via inhibition of the RNA-processing 59-39 exoribonucleases. Our results provide evidence for the role of chloroplast-derived signal and RNA metabolism in the control of cell death and biotic stress response.

Recent years have witnessed a breathtaking increase in the availability of genome sequence data, providing evidence of the highly duplicate nature of eukaryotic genomes. Plants are exceptional among eukaryotic organisms in that duplicate loci compose a large fraction of their genomes, partly because of the frequent occurrence of polyploidy (or whole-genome duplication) events. Tandem gene duplication and transposition have also contributed to the large number of duplicated genes in plant genomes. Evolutionary analyses allowed the dynamics of duplicate gene evolution to be studied and several models were proposed. It seems that, over time, many duplicated genes were lost and some of those that were retained gained new functions and/or expression patterns (neofunctionalization) or subdivided their functions and/or expression patterns between them (subfunctionalization). Recent studies have provided examples of genes that originated by duplication with successive diversification within plants. In this review, we focused on the TEL (TERMINAL EAR1-like) genes to illustrate such mechanisms. Emerged from the mei2 gene family, these TEL genes are likely to be land plant-specific. Phylogenetic analyses revealed one or two TEL copies per diploid genome. TEL gene degeneration and loss in several Angiosperm species such as in poplar and maize seem to have occurred. In Arabidopsis thaliana, whose genome experienced at least three polyploidy events followed by massive gene loss and genomic reorganization, two TEL genes were retained and two new shorter TEL-like (MCT) genes emerged. Molecular and expression analyses suggest for these genes sub- and neofunctionalization events, but confirmation will come from their functional characterization.

Programmed cell death (PCD) is essential for several aspects of plant life. We previously identified the mips1 mutant of Arabidopsis thaliana, which is deficient for the enzyme catalysing myo-inositol synthesis, and that displays light-dependent formation of lesions on leaves due to Salicylic Acid (SA) over-accumulation. Rationale of this work was to identify novel regulators of plant pcD using a genetic approach. A screen for secondary mutations that abolish the mips1 PCD phenotype identified a mutation in the BIG gene, encoding a factor of unknown molecular function that was previously shown to play pleiotropic roles in plant development and defence. physiological analyses showed that BiG is required for lesion formation in mips1 via SA-dependant signalling. big mutations partly rescued transcriptomic and metabolomics perturbations as stress-related phytohormones homeostasis. in addition, since loss of function of the ceramide synthase LOH2 was not able to abolish cell death induction in mips1, we show that pcD induction is not fully dependent of sphingolipid accumulation as previously suggested. our results provide further insights into the role of the BiG protein in the control of MIPS1-dependent cell death and also into the impact of sphingolipid homeostasis in this pathway. Myo-inositol (MI) is a ubiquitous molecule and the precursor for biosynthesis of many inositol-derivatives such as inositol phosphates, phosphatidylinositol (PtdIns) phosphate, or specific classes of sphingolipids that play critical and diverse roles in vesicle trafficking, hormone signalling, and biotic and abiotic stress responses 1, 2. The rate-limiting step of MI synthesis is catalysed by l-myo-inositol 1-phosphate synthase (MIPS), using Glucose-6-P as a substrate. This reaction is followed by dephosphorylation of l-myo-inositol 1-phosphate into MI. These two reactions together, called the Loewus pathway, are the only known route for MI biosynthesis 3. Three genes encoding MIPS isoforms have been identified in the Arabidopsis genome 4, 5 , among them MIPS1 is responsible for most of MI biosynthesis in leaves. Pleiotropic developmental defects such as reduced root growth or altered venation in cotyledons have been described for the mips1 loss of function mutant 6-8. One of its most striking features is the light intensity-dependent formation of leaf lesions due to Salicylic acid (SA)dependent Programmed Cell Death (PCD), revealing the importance of MI or inositol derivatives in the regulation of these processes. However, how light affects MIPS transcript level and inositol biosynthesis was an open question for a long time until the demonstration that the two light signalling proteins, FAR-RED ELONGATED HYPOCOTYL 3 (FHY3) and its homolog, FAR-RED IMPAIRED RESPONSE 1 (FAR1), were able to directly bind MIPS1 promoter and to activate its expression, thereby promoting inositol biosynthesis to prevent lightinduced SA-dependent cell death 9. Because MI is used to synthetize numerous compounds in the cell, including PtdIns, a link between mip...