Integrative Analysis of Transcriptomics and Metabolomics to Reveal the Melanogenesis Pathway of Muscle and Related Meat Characters in Wuliangshan Black-Boned Chickens

Background: Melanin is an important antioxidant in food, and has been used in medicine and cosmetology. Chicken meat with high melanin content from black-boned chickens have been considered a high nutritious food with potential medicinal properties. The molecular mechanism of melanogenesis of skeletal muscle in black-boned chickens remain poorly understood. This study investigated the biological gene-metabolite associations regulating the muscle melanogenesis pathways in Wuliangshan black-boned chickens with two normal boned chicken breeds as control.Results: We identified 25 differentially expressed genes and 11 transcription factors in the melanogenesis pathways. High levels of the meat flavor compounds inosine monophosphate, hypoxanthine, lysophospholipid, hydroxyoctadecadienoic acid, and nicotinamide mononucleotide were found in Wuliangshan black-boned chickens.Conclusion: Integrative analysis of transcriptomics and metabolomics revealed the dual physiological functions of the PDZK1 gene, involved in pigmentation and/or melanogenesis and regulating the phospholipid signaling processes in muscle of black boned chickens.

Rice Non-Specific Phospholipase C6 Is Involved in Mesocotyl Elongation

ABSTRACT Mesocotyl elongation of rice is crucial for seedlings pushing out of deep soil. Underlying mechanisms on the phospholipid signaling in mesocotyl growth of rice are elusive. Here we report that the rice non-specific phospholipase C6 (OsNPC6) is involved in the mesocotyl elongation. Our results indicated that all five rice OsNPCs (OsNPC1, OsNPC2, OsNPC3, OsNPC4 and OsNPC6) hydrolyzed the substrate phosphatidylcholine (PC) to phosphocholine (PCho), and all of them showed plasma membrane localization. Overexpression (OE) of OsNPC6 produced plants with shorter mesocotyls, while comparing to those of Nipponbare (Nip) and npc6 mutants. Although the mesocotyl growth of npc6 mutants was not much affected without GA3, it was obviously elongated by the treatment of GA. Upon GA3 treatment, SLENDER RICE1 (SLR1), the DELLA protein of gibberellin (GA) signaling, was drastically increased in OE plants, in contrary, the level of SLR1 was found decreased in npc6 mutants. The GA-enhanced mesocotyl elongation and the GA-impaired SLR1 level in npc6 mutants were attenuated by the supplementation of PCho. Further analysis indicated that the GA-induced expression of phospho-base N-methyltransferase 1 (PMT1) in npc6 mutants was significantly weakened by the addition of PCho. In summary, our results suggest that OsNPC6 is involved in mesocotyl development via modulation of phosphocholine in rice.

Phospholipid signaling pathway in Capsicum chinense suspension cells as a key response to consortium infection

Background Mexico is considered the diversification center for chili species, but these crops are susceptible to infection by pathogens such as Colletotrichum spp., which causes anthracnose disease and postharvest decay in general. Studies have been carried out with isolated strains of Colletotrichum in Capsicum plants; however, under growing conditions, microorganisms generally interact with others, resulting in an increase or decrease of their ability to infect the roots of C. chinense seedlings and thus, cause disease. Results Morphological changes were evident 24 h after inoculation (hai) with the microbial consortium, which consisted primarily of C. ignotum. High levels of diacylglycerol pyrophosphate (DGPP) and phosphatidic acid (PA) were found around 6 hai. These metabolic changes could be correlated with high transcription levels of diacylglycerol-kinase (CchDGK1 and CchDG31) at 3, 6 and 12 hai and also to pathogen gene markers, such as CchPR1 and CchPR5. Conclusions Our data constitute the first evidence for the phospholipids signalling events, specifically DGPP and PA participation in the phospholipase C/DGK (PI-PLC/DGK) pathway, in the response of Capsicum to the consortium, offering new insights on chilis’ defense responses to damping-off diseases.

DAF-18 is required for the age-dependent increase in DAF-16 activity in Caenorhabditis elegans

ABSTRACTThe insulin/insulin-like growth factor signaling (IIS) pathway modulates growth, survival, and lifespan by regulating FOXO transcription factors. In Caenorhabditis elegans, IIS maintains DAF-16/FOXO in an inactive state unless animals are challenged by environmental stress. Recent evidence suggests that DAF-16 becomes activated as part of normal aging in C. elegans, yet the regulatory module responsible for this phenomenon is largely undefined. Embedded within IIS is phospholipid signaling in which PIP3 produced by the PI3 kinase AGE-1 is an upstream event in DAF-16 inhibition. Countering AGE-1 is DAF-18, an ortholog of human PTEN phosphatase that dephosphorylates PIP3. Although it is required for normal lifespan in C. elegans, functional characterization of DAF-18 has primarily focused on its roles during development in the germline and neurons. In this study we asked whether DAF-18 plays a role in the age-dependent activation of DAF-16, and specifically in DAF-16-mediated immunity. Our data show that DAF-18 is expressed in multiple tissues during adulthood. We found that DAF-18 contributes to host defense in adult animals by functioning in the neurons and intestine, likely working through DAF-16 which acts in those same tissues to confer immunity. Supporting this possibility, DAF-18 was required for increased DAF-16 transcriptional activity during aging. Post-translational modifications including ubiquitination and sumoylation appear to be required for the function of DAF-18 during aging in C. elegans, indicating that strategies to modulate PTEN activity are evolutionarily conserved. Our results establish an important role for DAF-18 later in life and imply that it is a critical component of a neuroendocrine signaling circuit that governs the dynamic activity of DAF-16.

Phospholipid Signaling Is a Component of the Salicylic Acid Response in Plant Cell Suspension Cultures

Salicylic acid (SA) is an important signaling molecule involved in plant defense. While many proteins play essential roles in SA signaling, increasing evidence shows that responses to SA appear to involve and require lipid signals. The phospholipid-generated signal transduction involves a family of enzymes that catalyze the hydrolysis or phosphorylation of phospholipids in membranes to generate signaling molecules, which are important in the plant cellular response. In this review, we focus first, the role of SA as a mitigator in biotic/abiotic stress. Later, we describe the experimental evidence supporting the phospholipid–SA connection in plant cells, emphasizing the roles of the secondary lipid messengers (phosphatidylinositol 4,5-bisphosphate (PIP2) and phosphatidic acid (PA)) and related enzymes (phospholipase D (PLD) and phospholipase C (PLC)). By placing these recent finding in context of phospholipids and SA in plant cells, we highlight the role of phospholipids as modulators in the early steps of SA triggered transduction in plant cells.

Phosphatidylinositol-phospholipase C2 regulates pattern-triggered immunity in Nicotiana benthamiana

Phospholipid signaling plays an important role in plant immune responses against phytopathogenic bacteria in Nicotiana benthamiana. Here, we isolated two phospholipase C2 (PLC2) orthologs in the N. benthamiana genome, designated as PLC2-1 and 2-2. Both NbPLC2-1 and NbPLC2-2 were expressed in most tissues and were induced by infiltration with bacteria and flg22. NbPLC2-1 and NbPLC2-2 (NbPLC2s) double-silenced plants showed a moderately reduced growth phenotype. The induction of the hypersensitive response was not affected, but bacterial growth and the appearance of bacterial wilt were accelerated in NbPLC2s-silenced plants when they were challenged with a virulent strain of Ralstonia solanacearum that was compatible with N. benthamiana. NbPLC2s-silenced plants showed reduced expression levels of NbPR-4, a marker gene for jasmonic acid signaling, and decreased jasmonic acid and jasmonoyl-L-isoleucine contents after inoculation with R. solanacearum. The induction of pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI) marker genes was reduced in NbPLC2s-silenced plants after infiltration with R. solanacearum or Pseudomonas fluorescens. Accordingly, the resistance induced by flg22 was compromised in NbPLC2s-silenced plants. In addition, the expression of flg22-induced PTI marker genes, the oxidative burst, stomatal closure, and callose deposition were all reduced in the silenced plants. Thus, NbPLC2s might have important roles in pre- and post-invasive defenses, namely in the induction of PTI.

Phospholipid signaling pathway in Capsicum chinense suspension cells as a key response to a consortium infection

Mexico is considered to be a diversification center for the chili species, but at the same time, these crops have been susceptible to infection by pathogens, such as Colletotrichum, which causes anthracnose diseases and postharvest decay in general. Different studies have been carried out with isolated strains of Colletotrichum in Capsicum plants, however, under growing conditions, the microorganisms are interacting with others, which can increase or decrease their infective capacity. This study presents the first report between plant-pathogen interactions and their biochemical responses in phospholipid pathways for C. chinense to microbial consortium with mainly Colletotrichum ignotum pathogen. The results showed morphological changes in the first hours (h) in the presence of the microbial consortium, and high levels of diacylglycerol pyrophosphate (DGPP) and phosphatidic acid (PA) were found after 6 h postinoculation (hai). These metabolic changes were correlated with high transcription levels of diacylglycerol-kinase (CchDGKs) expressed for 3, 6 and 12 hai and related to pathogen gene markers, such as CchPR1 and CchPR5. Finally, this study shows how the phospholipase C/DGK (PLC/DGK) pathway offers insight into the microbial infection responses of chili crops with damping-off diseases in the Yucatan.

Synj1 haploinsufficiency causes dopamine neuron vulnerability and alpha-synuclein accumulation in mice

Synaptojanin1 (synj1) is a phosphoinositide phosphatase with dual SAC1 and 5′-phosphatase enzymatic activities in regulating phospholipid signaling. The brain-enriched isoform has been shown to participate in synaptic vesicle (SV) recycling. More recently, recessive human mutations were identified in the two phosphatase domains of SYNJ1, including R258Q, R459P and R839C, which are linked to rare forms of early-onset Parkinsonism. We now demonstrate that Synj1 heterozygous deletion (Synj1+/−), which is associated with an impaired 5′-phosphatase activity, also leads to Parkinson’s disease (PD)-like pathologies in mice. We report that male Synj1+/− mice display age-dependent motor function abnormalities as well as alpha-synuclein accumulation, impaired autophagy and dopaminergic terminal degeneration. Synj1+/− mice contain elevated 5′-phosphatase substrate, PI(4,5)P2, particularly in the midbrain neurons. Moreover, pharmacological elevation of membrane PI(4,5)P2 in cultured neurons impairs SV endocytosis, specifically in midbrain neurons, and further exacerbates SV trafficking defects in Synj1+/− midbrain neurons. We demonstrate down-regulation of SYNJ1 transcript in a subset of sporadic PD brains, implicating a potential role of Synj1 deficiency in the decline of dopaminergic function during aging.