Symbiotic signalling is at the core of an endophytic Fusarium solani-legume association

AbstractLegumes interact with a wide range of microbes in their root system, ranging from beneficial symbionts to pathogens. Symbiotic rhizobia and arbuscular mycorrhizal glomeromycetes trigger a so-called common symbiotic signalling pathway (CSSP), including the induction of nuclear calcium spiking in the root epidermis. In our study, the recognition of an endophytic Fusarium solani strain K in Lotus japonicus induced the expression of LysM receptors for chitin-based molecules, CSSP members and CSSP-dependent genes in L. japonicus. In LysM and CSSP mutant/RNAi lines, root penetration and fungal intraradical progression was either stimulated or limited while FsK exudates are perceived in a CSSP-dependent manner, triggering nuclear calcium spiking in epidermal cells of Medicago truncatula Root Organ Cultures. Our results corroborate that the CSSP is a more common pathway than previously envisaged, involved in the perception of signals from other microbes beyond the restricted group of symbiotic interactions sensu stricto.

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A Bacterial Tower of Babel: Quorum-Sensing Signaling Diversity and Its Evolution

Annual Review of Microbiology ◽

10.1146/annurev-micro-012220-063740 ◽

2020 ◽

Vol 74 (1) ◽

pp. 587-606 ◽

Cited By ~ 1

Author(s):

Nitzan Aframian ◽

Avigdor Eldar

Keyword(s):

Quorum Sensing ◽

Social Interactions ◽

Signal Molecules ◽

Allelic Polymorphism ◽

Dependent Manner ◽

Tower Of Babel ◽

Cognate Receptor ◽

Wide Range ◽

Family Code ◽

Bacterial Groups

Quorum sensing is a process in which bacteria secrete and sense a diffusible molecule, thereby enabling bacterial groups to coordinate their behavior in a density-dependent manner. Quorum sensing has evolved multiple times independently, utilizing different molecular pathways and signaling molecules. A common theme among many quorum-sensing families is their wide range of signaling diversity—different variants within a family code for different signal molecules with a cognate receptor specific to each variant. This pattern of vast allelic polymorphism raises several questions—How do different signaling variants interact with one another? How is this diversity maintained? And how did it come to exist in the first place? Here we argue that social interactions between signaling variants can explain the emergence and persistence of signaling diversity throughout evolution. Finally, we extend the discussion to include cases where multiple diverse systems work in concert in a single bacterium.

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Growth Promotion or Osmotic Stress Response: How SNF1-Related Protein Kinase 2 (SnRK2) Kinases Are Activated and Manage Intracellular Signaling in Plants

Plants ◽

10.3390/plants10071443 ◽

2021 ◽

Vol 10 (7) ◽

pp. 1443

Author(s):

Yoshiaki Kamiyama ◽

Sotaro Katagiri ◽

Taishi Umezawa

Keyword(s):

Protein Kinase ◽

Plant Growth ◽

Osmotic Stress ◽

Protein Function ◽

Intracellular Signaling ◽

Growth Promotion ◽

Research Field ◽

Dependent Manner ◽

Related Protein ◽

Wide Range

Reversible phosphorylation is a major mechanism for regulating protein function and controls a wide range of cellular functions including responses to external stimuli. The plant-specific SNF1-related protein kinase 2s (SnRK2s) function as central regulators of plant growth and development, as well as tolerance to multiple abiotic stresses. Although the activity of SnRK2s is tightly regulated in a phytohormone abscisic acid (ABA)-dependent manner, recent investigations have revealed that SnRK2s can be activated by group B Raf-like protein kinases independently of ABA. Furthermore, evidence is accumulating that SnRK2s modulate plant growth through regulation of target of rapamycin (TOR) signaling. Here, we summarize recent advances in knowledge of how SnRK2s mediate plant growth and osmotic stress signaling and discuss future challenges in this research field.

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CRL4-DCAF12 Ubiquitin Ligase Controls MOV10 RNA Helicase during Spermatogenesis and T Cell Activation

International Journal of Molecular Sciences ◽

10.3390/ijms22105394 ◽

2021 ◽

Vol 22 (10) ◽

pp. 5394

Author(s):

Tomas Lidak ◽

Nikol Baloghova ◽

Vladimir Korinek ◽

Radislav Sedlacek ◽

Jana Balounova ◽

...

Keyword(s):

T Cell ◽

T Cell Activation ◽

Ubiquitin Ligase ◽

Cell Activation ◽

Rna Helicase ◽

Dependent Manner ◽

Amino Acid Residues ◽

Risc Complex ◽

Wide Range

Multisubunit cullin-RING ubiquitin ligase 4 (CRL4)-DCAF12 recognizes the C-terminal degron containing acidic amino acid residues. However, its physiological roles and substrates are largely unknown. Purification of CRL4-DCAF12 complexes revealed a wide range of potential substrates, including MOV10, an “ancient” RNA-induced silencing complex (RISC) complex RNA helicase. We show that DCAF12 controls the MOV10 protein level via its C-terminal motif in a proteasome- and CRL-dependent manner. Next, we generated Dcaf12 knockout mice and demonstrated that the DCAF12-mediated degradation of MOV10 is conserved in mice and humans. Detailed analysis of Dcaf12-deficient mice revealed that their testes produce fewer mature sperms, phenotype accompanied by elevated MOV10 and imbalance in meiotic markers SCP3 and γ-H2AX. Additionally, the percentages of splenic CD4+ T and natural killer T (NKT) cell populations were significantly altered. In vitro, activated Dcaf12-deficient T cells displayed inappropriately stabilized MOV10 and increased levels of activated caspases. In summary, we identified MOV10 as a novel substrate of CRL4-DCAF12 and demonstrated the biological relevance of the DCAF12-MOV10 pathway in spermatogenesis and T cell activation.

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Zebrafish Blunt-Force TBI Induces Heterogenous Injury Pathologies That Mimic Human TBI and Responds with Sonic Hedgehog-Dependent Cell Proliferation across the Neuroaxis

Biomedicines ◽

10.3390/biomedicines9080861 ◽

2021 ◽

Vol 9 (8) ◽

pp. 861

Author(s):

James Hentig ◽

Kaylee Cloghessy ◽

Manuela Lahne ◽

Yoo Jin Jung ◽

Rebecca A. Petersen ◽

...

Keyword(s):

Cell Proliferation ◽

Proliferative Response ◽

Injury Severity ◽

Granule Cell Layer ◽

Dependent Manner ◽

Adult Zebrafish ◽

Post Injury ◽

Blunt Force ◽

Shh Pathway ◽

Wide Range

Blunt-force traumatic brain injury (TBI) affects an increasing number of people worldwide as the range of injury severity and heterogeneity of injury pathologies have been recognized. Most current damage models utilize non-regenerative organisms, less common TBI mechanisms (penetrating, chemical, blast), and are limited in scalability of injury severity. We describe a scalable blunt-force TBI model that exhibits a wide range of human clinical pathologies and allows for the study of both injury pathology/progression and mechanisms of regenerative recovery. We modified the Marmarou weight drop model for adult zebrafish, which delivers a scalable injury spanning mild, moderate, and severe phenotypes. Following injury, zebrafish display a wide range of severity-dependent, injury-induced pathologies, including seizures, blood–brain barrier disruption, neuroinflammation, edema, vascular injury, decreased recovery rate, neuronal cell death, sensorimotor difficulties, and cognitive deficits. Injury-induced pathologies rapidly dissipate 4–7 days post-injury as robust cell proliferation is observed across the neuroaxis. In the cerebellum, proliferating nestin:GFP-positive cells originated from the cerebellar crest by 60 h post-injury, which then infiltrated into the granule cell layer and differentiated into neurons. Shh pathway genes increased in expression shortly following injury. Injection of the Shh agonist purmorphamine in undamaged fish induced a significant proliferative response, while the proliferative response was inhibited in injured fish treated with cyclopamine, a Shh antagonist. Collectively, these data demonstrate that a scalable blunt-force TBI to adult zebrafish results in many pathologies similar to human TBI, followed by recovery, and neuronal regeneration in a Shh-dependent manner.

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A Fish Galectin-8 Possesses Direct Bactericidal Activity

International Journal of Molecular Sciences ◽

10.3390/ijms22010376 ◽

2020 ◽

Vol 22 (1) ◽

pp. 376

Author(s):

Tengfei Zhang ◽

Shuai Jiang ◽

Li Sun

Keyword(s):

Bactericidal Activity ◽

Bacterial Pathogens ◽

Bactericidal Effect ◽

Immune Defense ◽

Carbohydrate Binding ◽

Dependent Manner ◽

Animal Cells ◽

Gram Negative ◽

Tongue Sole ◽

Wide Range

Galectins are a family of animal lectins with high affinity for β-galactosides. Galectins are able to bind to bacteria, and a few mammalian galectins are known to kill the bound bacteria. In fish, no galectins with direct bactericidal effect have been reported. In the present study, we identified and characterized a tandem repeat galectin-8 from tongue sole Cynoglossus semilaevis (designated CsGal-8). CsGal-8 possesses conserved carbohydrate recognition domains (CRDs), as well as the conserved HXNPR and WGXEE motifs that are critical for carbohydrate binding. CsGal-8 was constitutively expressed in nine tissues of tongue sole and up-regulated in kidney, spleen, and blood by bacterial challenge. When expressed in HeLa cells, CsGal-8 protein was detected both in the cytoplasm and in the micro-vesicles secreted from the cells. Recombinant CsGal-8 (rCsGal-8) bound to lactose and other carbohydrates in a dose dependent manner. rCsGal-8 bound to a wide range of gram-positive and gram-negative bacteria and was co-localized with the bound bacteria in animal cells. Lactose, fructose, galactose, and trehalose effectively blocked the interactions between rCsGal-8 and different bacteria. Furthermore, rCsGal-8 exerted potent bactericidal activity against some gram-negative bacterial pathogens by directly damaging the membrane and structure of the pathogens. Taken together, these results indicate that CsGal-8 likely plays an important role in the immune defense against some bacterial pathogens by direct bacterial interaction and killing.

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Abstract 316: A Potential Mechanism Involving mTOR For The Expression Of CTGF In Agonist-stimulated Adult Cardiomyocytes

Circulation Research ◽

10.1161/res.113.suppl_1.a316 ◽

2013 ◽

Vol 113 (suppl_1) ◽

Author(s):

Kamala P Sundararaj ◽

Sundaravadivel Balasubramanian ◽

Dorea Pleasant ◽

Dhandapani Kuppuswamy

Keyword(s):

Mrna Expression ◽

Wound Repair ◽

Cardiac Fibrosis ◽

Interstitial Fibrosis ◽

Treatment Options ◽

Tissue Growth ◽

Dependent Manner ◽

Potential Mechanism ◽

Wall Stiffness ◽

Wide Range

Cardiac hypertrophy ensues as a response to multiple stimuli, such as mechanical stress, neurohumoral activation, growth factors and cytokines. Connective Tissue Growth Factor (CTGF), a potent fibrogenic cytokine, regulates a wide range of biological functions including ECM deposition, wound repair, angiogenesis, migration, differentiation, survival and proliferation. While CTGF overexpression in fibroblasts has been shown to be responsible for fibrosis in various organs, controversy exists about the source of CTGF. Since interstitial fibrosis contributes to ventricular wall stiffness and impairs diastolic function, understating how key factors such as CTGF are expressed and released for the genesis of fibrosis in the hypertrophying heart is important to develop new treatment options. To this end, we explored the signaling pathway(s) involved in the phenylephrine (PE), a hypertrophic agonist, induced expression of CTGF by cardiomyocytes (CMs). Since mammalian target of rapamycin (mTOR) is reported to regulate PE-induced hypertrophic signaling, we hypothesize that mTOR plays a role in PE induced CTGF expression in CMs. To test if CMs produce CTGF, we treated adult feline CMs with phenylephrine. PE stimulated CTGF mRNA expression in a dose and time dependent manner. mTOR forms two distinct complexes, mTORC1 and mTORC2. Whereas both complexes are sensitive to a pharmacological inhibitor Torin1, only mTORC1 is sensitive to Rapamycin inhibition. Our results indicate that PE stimulated CTGF expression could be substantially enhanced by torin1 pretreatment of CMs. Moreover, shRNA mediated silencing of Rictor in CMs, one of the components of mTORC2, significantly augmented the PE induced CTGF mRNA expression. But mTORC1 inhibition using Rapamycin or activation of its downstream target S6K1 using Rapamycin resistant S6K1 adenovirus had no impact in PE -stimulated CTGF expression. The same trend was also observed in the level of secreted CTGF. In conclusion, these results strongly indicate that mTORC2 plays a repressive role in CTGF mRNA expression in adult CMs, and that the loss of such repression in PO myocardium might be a potential mechanism for the onset of cardiac fibrosis in hypertrophying myocardium.

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Echinococcus spp.: Tapeworms that Pose a Danger to Both Animals and Humans – a Review

Scientia Agriculturae Bohemica ◽

10.1515/sab-2017-0026 ◽

2017 ◽

Vol 48 (4) ◽

pp. 193-201 ◽

Cited By ~ 1

Author(s):

A. Brožová ◽

I. Jankovská ◽

V. Bejček ◽

S. Nechybová ◽

P. Peřinková ◽

...

Keyword(s):

Small Intestine ◽

Life Cycle ◽

Echinococcus Multilocularis ◽

Alveolar Echinococcosis ◽

Sensu Stricto ◽

Mammal Species ◽

Current State ◽

Wide Range ◽

The World ◽

Echinococcus Spp

Abstract Species of the genus Echinococcus (Cestoda; Taeniidae) are minute tapeworms of carnivores. Their larvae are known as hydatids (metacestode), which proliferate asexually in various mammals. Like the majority of cestodes, Echinococcus spp. require two different host species to complete their life cycle. Definitive hosts harbouring the adult cestodes in the small intestine are exclusively carnivores of the Canidae and Felidae families. A wide range of mammal species including humans is susceptible to infection by the metacestode of Echinococcus spp., which develops in their viscera. The disease, caused by species of the genus Echinococcus, is called echinococcosis, and it is one of the most dangerous zoonoses in the world. The traditional species Echinococcus granulosus and Echinococcus multilocularis are agents of significant diseases due to the high number of cases and the wide geographical species range. The taxonomy of the genus is controversial; in the current state of ongoing complex revisions, the agent of cystic echinococcosis E. granulosus sensu lato is divided into five species (E. granulosus sensu stricto, E. felidis, E. equinus, E. ortleppi, E. canadensis), in addition to the agents of alveolar echinococcosis (E. multilocularis, E. shiquicus) and polycystic/unicystic echinococcosis (E. vogeli, E. oligarthrus). Here we provide an overview of the current situation, which continues to develop.

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Inhibiting myosin-ATPase reveals a dynamic range of mitochondrial respiratory control in skeletal muscle

Biochemical Journal ◽

10.1042/bj20110366 ◽

2011 ◽

Vol 437 (2) ◽

pp. 215-222 ◽

Cited By ~ 93

Author(s):

Christopher G. R. Perry ◽

Daniel A. Kane ◽

Chien-Te Lin ◽

Rachel Kozy ◽

Brook L. Cathey ◽

...

Keyword(s):

Skeletal Muscle ◽

Dynamic Range ◽

Energy Charge ◽

Respiratory Control ◽

Basic Research ◽

Dependent Manner ◽

Atpase Inhibitor ◽

Wide Range ◽

The Impact

Assessment of mitochondrial ADP-stimulated respiratory kinetics in PmFBs (permeabilized fibre bundles) is increasingly used in clinical diagnostic and basic research settings. However, estimates of the Km for ADP vary considerably (~20–300 μM) and tend to overestimate respiration at rest. Noting that PmFBs spontaneously contract during respiration experiments, we systematically determined the impact of contraction, temperature and oxygenation on ADP-stimulated respiratory kinetics. BLEB (blebbistatin), a myosin II ATPase inhibitor, blocked contraction under all conditions and yielded high Km values for ADP of >~250 and ~80 μM in red and white rat PmFBs respectively. In the absence of BLEB, PmFBs contracted and the Km for ADP decreased ~2–10-fold in a temperature-dependent manner. PmFBs were sensitive to hyperoxia (increased Km) in the absence of BLEB (contracted) at 30 °C but not 37 °C. In PmFBs from humans, contraction elicited high sensitivity to ADP (Km<100 μM), whereas blocking contraction (+BLEB) and including a phosphocreatine/creatine ratio of 2:1 to mimic the resting energetic state yielded a Km for ADP of ~1560 μM, consistent with estimates of in vivo resting respiratory rates of <1% maximum. These results demonstrate that the sensitivity of muscle to ADP varies over a wide range in relation to contractile state and cellular energy charge, providing evidence that enzymatic coupling of energy transfer within skeletal muscle becomes more efficient in the working state.

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In vitro analysis of a transcription termination site for RNA polymerase II.

Molecular and Cellular Biology ◽

10.1128/mcb.10.11.5782 ◽

1990 ◽

Vol 10 (11) ◽

pp. 5782-5795 ◽

Cited By ~ 19

Author(s):

D K Wiest ◽

D K Hawley

Keyword(s):

Rna Polymerase ◽

Rna Polymerase Ii ◽

Dna Sequences ◽

Nuclear Extract ◽

Transcription Unit ◽

Dependent Manner ◽

Wide Range ◽

Vitro Analysis

Transcription from the adenovirus major late (ML) promoter has previously been shown to pause or terminate prematurely in vivo and in vitro at a site within the first intron of the major late transcription unit. We are studying the mechanism of elongation arrest at this site in vitro to define the DNA sequences and proteins that determine the elongation behavior of RNA polymerase II. Our assay system consists of a nuclear extract prepared from cultured human cells. With standard reaction conditions, termination is not observed downstream of the ML promoter. However, in the presence of Sarkosyl, up to 80% of the transcripts terminate 186 nucleotides downstream of the start site. Using this assay, we showed that the DNA sequences required to promote maximal levels of termination downstream of the ML promoter reside within a 65-base-pair region and function in an orientation-dependent manner. To test whether elongation complexes from the ML promoter were functionally homogeneous, we determined the termination efficiency at each of two termination sites placed in tandem. We found that the behavior of the elongation complexes was different at these sites, with termination being greater at the downstream site over a wide range of Sarkosyl concentrations. This result ruled out a model in which the polymerases that read through the first site were stably modified to antiterminate. We also demonstrated that the ability of the elongation complexes to respond to the ML termination site was promoter specific, as the site did not function efficiently downstream of a heterologous promoter. Taken together, the results presented here are not consistent with the simplest class of models that have been proposed previously for the mechanism of Sarkosyl-induced termination.

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A Possible Role of Allatostatin C in Inhibiting Ecdysone Biosynthesis Revealed in the Mud Crab Scylla paramamosain

Frontiers in Marine Science ◽

10.3389/fmars.2021.740251 ◽

2021 ◽

Vol 8 ◽

Author(s):

An Liu ◽

Wenyuan Shi ◽

Dongdong Lin ◽

Haihui Ye

Keyword(s):

Scylla Paramamosain ◽

Dependent Manner ◽

Mud Crab ◽

Methyl Farnesoate ◽

Independent Manner ◽

Wide Range ◽

Negative Effect

C-type allatostatins (C-type ASTs) are a family of structurally related neuropeptides found in a wide range of insects and crustaceans. To date, the C-type allatostatin receptor in crustaceans has not been deorphaned, and little is known about its physiological functions. In this study, we aimed to functionally define a C-type ASTs receptor in the mud crab, Scylla paramamosian. We showed that C-type ASTs receptor can be activated by ScypaAST-C peptide in a dose-independent manner and by ScypaAST-CCC peptide in a dose-dependent manner with an IC50 value of 6.683 nM. Subsequently, in vivo and in vitro experiments were performed to investigate the potential roles of ScypaAST-C and ScypaAST-CCC peptides in the regulation of ecdysone (20E) and methyl farnesoate (MF) biosynthesis. The results indicated that ScypaAST-C inhibited biosynthesis of 20E in the Y-organ, whereas ScypaAST-CCC had no effect on the production of 20E. In addition, qRT-PCR showed that both ScypaAST-C and ScypaAST-CCC significantly decreased the level of expression of the MF biosynthetic enzyme gene in the mandibular organ, suggesting that the two neuropeptides have a negative effect on the MF biosynthesis in mandibular organs. In conclusion, this study provided new insight into the physiological roles of AST-C in inhibiting ecdysone biosynthesis. Furthermore, it was revealed that AST-C family peptides might inhibit MF biosynthesis in crustaceans.

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