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In this paper, we identified 32 putative polyprenyl synthase genes from whole genome databases of tomato and three tobacco varieties TN90, K and BX by using bioinformatics tools. Phylogenetic tree analysis showed that all genes were divided into three major clades, and four types of genes have been inferred as the reference of all functioned A.
Results showed that putative genes in polyprenyl synthase gene family included ggpps, fps, sps and gps, respectively. In view of phylogenetic relationships of four gene types, we found that gps and sps genes shared close relationship, which might be the result of recent gene duplication and divergence from a common ancestral sequence.
For ggpps genes, showed that 5 A. Previous reports identified 12 ggpps genes in whole genome of A. In phylogenetic analysis of this paper Figure 1 , we showed that all genes of GGPPS1 to GGPPS 11 were grouped as a single clade, which indicated that these genes may diverge from recent genome duplication events. Two differently expressed fps genes have been identified in whole genome of A. Phylogenetic analysis Figure 1 showed that these two genes were grouped as a single clade of Sub II, which was consistent with the high sequence similarity previously reported [ 10 ].
One significant gene duplication event divided all fps like genes of Nicotiana genus into two subclades Figures 1 and 3. However, fps genes of tomato were absent in one of the clade D1a of Figure 3. For tomato, the absence could again be due to the genome sequencing and assembly gaps; it is also conceivable that no gene duplication event took place for tomato fps subfamily.
Two sps and one gps genes, which shared close relationship in phylogenetic analysis, were identified in whole genome of A. We also identified some sequences of tomato and three tobacco varieties, which were grouped into A. We inferred that the close relationship may be due to recent gene duplication and divergence from common ancestral sequence gps and sps.
Molecular evolution analyses were performed in this paper to clarify the evolution characteristics of each subfamily. We could not find positive selection sites in GGPPS and FPS groups, which indicated that these genes may be important for biological processes and thus evolved conservatively. However, we detected two sites evolved under positive selection pressures in groups which contained sps and gps genes.
Positive selection sites identification indicated that some available mutations were retained in the evolution pathway, and these sites may be important for functions of protein [ 31 , 32 ]. We also found one of positive selection sites was neighbor to conserved domain of protein, suggesting its possibly important roles played in GGPPS and GPS enzymatic functioning. In summary, we identified putative polyprenyl synthase genes from whole genome of tomato and three tobacco varieties by using in silico methods.
Phylogenetic and multiple alignments analysis divided all polyprenyl synthase genes into three major clades and four subfamilies. Besides we preformed molecular evolution analysis to highlight evolution characteristics of these genes. Based on this paper, we provide data which should be important for further analysis of terpenoids biosynthesis in Solanaceae.
Acknowledgement The authors thank the Zhengzhou Tobacco Research Institute for support offered during the preliminary study. Advances in plant genome sequencing. Plant J. Langenheim JH. Higher plant terpenoids: Aphytocentric overview of their ecological roles. McCaskill D, Croteau R.
Procedures for the isolation and quantification of the intermediates of the mevalonic acid pathway. Anal Biochem. Isoprenoid biosynthesis via the methylerythritol phosphate pathway. Mechanistic investigations of the 1-deoxy-D-xylulose 5-phosphate reductoisomerase. Pfam: The protein families database. Nucleic Acids Res. Identification and subcellular localization of two solanesyldiphosphate synthases from Arabidopsis thaliana.
Plant Cell Physiol. Geranyldiphosphate synthase: cloning, expression and characterization of this prenyltransferase as a heterodimer. ProcNatlAcad Sci. Geranyldiphosphate synthase is required for biosynthesis of gibberellins. Farnesyldiphosphate synthase assay. Methods Mol Biol. Arabidopsis thaliana contains two differentially expressed farnesyl-diphosphate synthase genes.
J Biol Chem. The Arabidopsis thaliana FPP synthase isozymes have overlapping and specific functions in isoprenoid biosynthesis and complete loss of FPP synthase activity causes early developmental arrest. LEFPS1, a tomato farnesyl pyrophosphate gene highly expressed during early fruit development. Plant Physiol. Plant Mol Biol. Genome-wide identification and analysis of membrane-bound O-acyltransferase. MBOAT gene family in plants. The Pfam protein families database.
ProbCons: Probabilistic consistency-based multiple sequence alignment. Genome Res. BMC Bioinformatics. MEGA6: Molecular evolutionary genetics analysis version 6. Bayesian inference of phylogeny and its impact on evolutionary biology.
MrBayes 3. Syst Biol. DeLano WL. The PyMOL molecular graphics system. The tobacco genome sequence and its comparison with those of tomato and potato. Nature Communications. Identification of the GGPS1 genes encoding geranylgeranyldiphosphate synthases from mouse and human. For Qless SN D , residue retains a hydrogen bond to the carbonyl oxygen of S but loses the hydrogen bond to the side chain of N Instead, N inappropriately hydrogen bonds to Y and to D in the catalytic site.
This technique can be used to mark neural clones derived from individual neuroblasts, which divide asymmetrically to self-renew and to generate differentiated neurons and glia Betschinger and Knoblich, ; Sousa-Nunes et al. Extensive MARCM analysis of mutant neuroblast clones indicated that the qless and qless alleles produce very similar phenotypes.
Postembryonic loss of Qless activity in the optic lobe, central brain or thoracic neuromeres resulted in a dramatic reduction in neuroblast clonal growth by 96 hours after larval hatching ALH Fig. This clearly demonstrates that qless is required for neural growth, but this could be accounted for via primary effects upon cell proliferation, cell survival or both. Dietary supplementation with CoQ4, CoQ9 or CoQ10 rescues qless neural undergrowth Many different protein and nonprotein substrates for prenyl transferases have been described.
To determine whether the substrate for the Qless prenyl transferase is indeed CoQ, we induced wild-type and qless mutant clones in larvae raised on a diet supplemented with CoQ10 see Methods. CoQ10 supplementation did not significantly alter the average number of cells per clone clone size in wild-type neuroblast clones at 96 hours ALH Fig.
This indicates that augmenting the larval diet with CoQ10 cannot boost neural cell proliferation above the wild-type limit. Nevertheless, counts of the numbers of clones per CNS in central brain or thoracic neuromere regions revealed a threefold increase in clone frequency supplementary material Fig.
This strongly suggests that CoQ10 supplementation increases FLP recombinase activity and, although the underlying mechanism is not yet clear, it might provide a useful experimental tool for increasing the frequency of FLP-induced mitotic clones. These results demonstrate that qless undergrowth results from a CoQ deficiency and, together with the sequence analysis, they show that qless encodes the predicted PDSS1-like prenyl transferase required for the biosynthesis of active CoQ.
To assess whether the length of the CoQ isoprenoid chain is crucial for rescuing qless activity, we next performed dietary supplementation with CoQ9, the major CoQ isoform in rodents, and also with CoQ4, a synthetic isoform with a side chain that is shorter than that of any of the naturally occurring CoQ major isoforms.
This indicates that CoQ activity in the developing Drosophila CNS can be provided by lipid side chains of four to ten isoprenoid units long. View large Download slide qless neuroblast clones undergrow and can be rescued by dietary CoQ. Qless protects against mitochondrial stress and caspase activation To investigate the mechanism by which CoQ promotes the growth of neuroblast lineages, we first addressed whether qless is required for cell survival.
Immunostaining with CM1 antibody, which recognizes activated caspases in Drosophila, revealed that most neurons present in qless mutant clones at 96 hours ALH were undergoing caspase-mediated apoptosis Fig. Given that CoQ is a known component of mitochondria, we next examined the expression of Hsp60A, a molecular chaperone localizing to the inner mitochondrial membrane, where CoQ participates in the electron transport chain Baena-Lopez et al.
Hsp60A is known to be upregulated during mitochondrial stress triggered by high temperature or toxin-induced cell death. Hence, qless is required to protect neural cells against mitochondrial stress and caspase-mediated apoptosis.
View large Download slide Qless activity protects against mitochondrial stress and caspase activation. B OL clone showing nlsGFP-labelled cells expressing higher levels of the Hsp60A mitochondrial stress marker than surrounding cells outside the clone. In mammals, mitochondrial stresses can trigger release of pro-apoptotic proteins such as cytochrome c from the mitochondrial intermembrane space into the cytoplasm.
Although cytochrome c is essential for caspase activation in mammals, it is not required for most types of apoptosis in Drosophila Dorstyn et al. Drosophila cytochrome c also behaves differently from its mammalian counterpart in that several studies have shown that it remains localized to mitochondria during apoptosis Dorstyn et al.
However, this species difference is not absolute as other Drosophila studies show that cytochrome c becomes cytosolic during some types of apoptosis Abdelwahid et al. To determine which mechanism occurs during the apoptosis of CoQ-deficient neurons, we examined cytochrome c localization in qless mutant clones. We observed cytochrome c puncta in both wild-type and qless neurons Fig. However, punctate cytochrome c expression was markedly increased in qless neurons and this colocalized with the mitochondrial marker Hsp60A Fig.
This suggests that the bulk of cytochrome c remains localized to mitochondria during the apoptosis of qless neurons. As with other aspects of the qless neural phenotype, cytochrome c and Hsp60A upregulation was rescued by dietary supplementation with CoQ10 data not shown. Together, the mitochondrial analysis demonstrates that Qless prevents mitochondrial stress and promotes cell survival. Qless is required primarily for cell survival not cell proliferation To explain fully the qless undergrowth phenotype, it is necessary to distinguish whether CoQ activity is primarily required to prevent cell apoptosis or whether it might also have a direct input into cell growth and cell proliferation.
We therefore tested the effects of blocking apoptosis by using MARCM to express p35, an inhibitor of caspase activation, specifically within qless mutant clones UAS-p35; qless Surprisingly, however, blocking caspase activation was able to rescue efficiently the number of cells per qless mutant clone Fig.
This implies that the progenitors responsible for generating the rescued cells are themselves also rescued by p35 expression. Importantly, rescue of clone size by caspase inhibition also demonstrates that larval activity of qless is required primarily for neural cell survival rather than for cell growth and proliferation.
Our Drosophila Qless analysis has now demonstrated that the serine residue or threonine in humans that is located ten amino acids away from the first DDxxD catalytic site is also crucial for CoQ prenyl transferase activity in vivo. Structural modelling suggests that a serine or threonine residue is necessary at this position to prevent inappropriate interactions with the nearby catalytic site. As the human PDSS1 mutation is associated with early-onset neural pathologies, we focused in this study on qless functions in the developing CNS.
However, the qless Drosophila phenotype is not restricted to the CNS data not shown and so might also prove useful for modelling primary CoQ deficiencies in non-neural tissues. Moreover, as the Drosophila genome also encodes an orthologue of PDSS2, future studies might also shed light on the functions of the other subunit of the mammalian prenyl transferase holoenzyme, which is associated with Leigh syndrome in humans and with nephropathy in both humans and mice Lopez et al. View large Download slide p35 rescues neuroblast clonal growth but not mitochondrial disruption.
CoQ deficiency induces mitochondrial stress, caspase activation and neuronal apoptosis The primary CoQ deficiency associated with loss of Qless activity induced elevated expression of Hsp60A and cytochrome c, indicating increased mitochondrial stress.
This stress was associated with caspase activation and the caspase-dependent apoptosis of neurons. The observation that punctate cytochrome c expression remained elevated when caspase activity was blocked strongly suggests that the sequence of events is the following: loss of CoQ leads to increased mitochondrial stress, in turn triggering caspase activation and thus apoptosis.
We were surprised to observe that blocking caspase activation using p35 was enough to provide efficient rescue of the number of progeny cells generated by each qless mutant neuroblast. This result demonstrates clearly that qless activity is required in a cell-autonomous manner during larval stages primarily for neural cell survival rather than for neuroblast growth and division.
The question then arises as to how pexpressing qless mutant neuroblasts are able to grow and divide in the apparent absence of a normally functioning mitochondrial electron transport chain. One possible explanation is that the ATP needed to power neuroblast growth and division might be mostly generated by CoQ-independent cytoplasmic glycolysis rather than by CoQ-dependent mitochondrial oxidative phosphorylation.
Although future neuroblast studies will be needed to test this hypothesis directly, we note that there is a well-studied precedent in the case of cancer cells Vander Heiden et al. Rescue of Qless with dietary CoQ The undergrowth of qless mutant neuroblast clones was efficiently rescued by CoQ dietary supplementation. As CoQ supplementation did not lead to enlarged wild-type neuroblast clones, it seems that CoQ in our laboratory larval diet is not growth limiting.
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|Ddxxd motif investing||Two key isoprenoids, farnesyl pyrophosphate FPP and geranylgeranyl pyrophosphate GGPP are responsible for the post-translational prenylation of small GTP-binding proteins, and serve as the biosynthetic precursors to numerous other biomolecules. Plant Mol Biol. Many of these analogs were reported to exhibit SQS inhibition activity in the low nanomolar or picomolar range Brown et al. The X-ray structure of the S. Messenger RNA levels were very low in normal fibroblasts and lymphoblastoid cell lines, precluding comparison with CoQdeficient cells. To develop a genetically amenable model for primary CoQ deficiency, we isolated mutations in a previously uncharacterized Drosophila gene encoding an orthologue of human PDSS1.|
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