Integrated de novo Analysis of Transcriptional and Metabolic Variations in Salt-Treated Solenostemma argel Desert Plants

Solenostemma argel (Delile) Hayne is a desert plant that survives harsh environmental conditions with several vital medicinal properties. Salt stress is a major constraint limiting agricultural production around the globe. However, response mechanisms behind the adaptation of S. argel plants to salt stress are still poorly understood. In the current study, we applied an omics approach to explore how this plant adapts to salt stress by integrating transcriptomic and metabolomic changes in the roots and leaves of S. argel plants under salt stress. De novo assembly of transcriptome produced 57,796 unigenes represented by 165,147 transcripts/isoforms. A total of 730 differentially expressed genes (DEGs) were identified in the roots (396 and 334 were up- and down-regulated, respectively). In the leaves, 927 DEGs were identified (601 and 326 were up- and down-regulated, respectively). Gene ontology and Kyoto Encyclopedia of Genes And Genomes pathway enrichment analyses revealed that several defense-related biological processes, such as response to osmotic and oxidative stress, hormonal signal transduction, mitogen-activated protein kinase signaling, and phenylpropanoid biosynthesis pathways are the potential mechanisms involved in the tolerance of S. argel plants to salt stress. Furthermore, liquid chromatography-tandem mass spectrometry was used to detect the metabolic variations of the leaves and roots of S. argel under control and salt stress. 45 and 56 critical metabolites showed changes in their levels in the stressed roots and leaves, respectively; there were 20 metabolites in common between the roots and leaves. Differentially accumulated metabolites included amino acids, polyamines, hydroxycinnamic acids, monolignols, flavonoids, and saccharides that improve antioxidant ability and osmotic adjustment of S. argel plants under salt stress. The results present insights into potential salt response mechanisms in S. argel desert plants and increase the knowledge in order to generate more tolerant crops to salt stress.

Larval metamorphosis is inhibited by methimazole and propylthiouracil that reveals possible hormonal action in the mussel Mytilus coruscus

Larval metamorphosis in bivalves is a key event for the larva-to-juvenile transformation. Previously we have identified a thyroid hormone receptor (TR) gene that is crucial for larvae to acquire “competence” for the metamorphic transition in the mussel Mytilus courscus (Mc). The mechanisms of thyroid signaling in bivalves are still largely unknown. In the present study, we molecularly characterized the full-length of two iodothyronine deiodinase genes (McDx and McDy). Phylogenetic analysis revealed that deiodinases of molluscs (McDy, CgDx and CgDy) and vertebrates (D2 and D3) shared a node representing an immediate common ancestor, which resembled vertebrates D1 and might suggest that McDy acquired specialized function from vertebrates D1. Anti-thyroid compounds, methimazole (MMI) and propylthiouracil (PTU), were used to investigate their effects on larval metamorphosis and juvenile development in M. coruscus. Both MMI and PTU significantly reduced larval metamorphosis in response to the metamorphosis inducer epinephrine. MMI led to shell growth retardation in a concentration-dependent manner in juveniles of M. coruscus after 4 weeks of exposure, whereas PTU had no effect on juvenile growth. It is hypothesized that exposure to MMI and PTU reduced the ability of pediveliger larvae for the metamorphic transition to respond to the inducer. The effect of MMI and PTU on larval metamorphosis and development is most likely through a hormonal signal in the mussel M. coruscus, with the implications for exploring the origins and evolution of metamorphosis.

Ambulacrarian insulin-related peptides and their putative receptors suggest how insulin and similar peptides may have evolved from insulin-like growth factor

Background Some insulin/IGF-related peptides (irps) stimulate a receptor tyrosine kinase (RTK) that transfers the extracellular hormonal signal into an intracellular response. Other irps, such as relaxin, do not use an RTK, but a G-protein coupled receptor (GPCR). This is unusual since evolutionarily related hormones typically either use the same or paralogous receptors. In arthropods three different irps, i.e. arthropod IGF, gonadulin and Drosophila insulin-like peptide 7 (dilp7), likely evolved from a gene triplication, as in several species genes encoding these three peptides are located next to one another on the same chromosomal fragment. These arthropod irps have homologs in vertebrates, suggesting that the initial gene triplication was perhaps already present in the last common ancestor of deuterostomes and protostomes. It would be interesting to know whether this is indeed so and how insulin might be related to this trio of irps. Methodology Genes encoding irps as well as their putative receptors were identified in genomes and transcriptomes from echinoderms and hemichordates. Results A similar triplet of genes coding for irps also occurs in some ambulacrarians. Two of these are orthologs of arthropod IGF and dilp7 and the third is likely a gonadulin ortholog. In echinoderms, two novel irps emerged, gonad stimulating substance (GSS) and multinsulin, likely from gene duplications of the IGF and dilp7-like genes respectively. The structures of GSS diverged considerably from IGF, which would suggest they use different receptors from IGF, but no novel irp receptors evolved. If IGF and GSS use different receptors, and the evolution of GSS from a gene duplication of IGF is not associated with the appearance of a novel receptor, while irps are known to use two different types of receptors, the ancestor of GSS and IGF might have acted on both types of receptors while one or both of its descendants act on only one. There are three ambulacrarian GPCRs that have amino acid sequences suggestive of being irp GPCRs, two of these are orthologs of the gonadulin and dilp7 receptors. This suggests that the third might be an IGF receptor, and that by deduction, GSS only acts on the RTK. The evolution of GSS from IGF may represent a pattern, where IGF gene duplications lead to novel genes coding for shorter peptides that activate an RTK. It is likely this is how insulin and the insect neuroendocrine irps evolved independently from IGF. Conclusion The local gene triplication described from arthropods that yielded three genes encoding irps was already present in the last common ancestor of protostomes and deuterostomes. It seems plausible that irps, such as those produced by neuroendocrine cells in the brain of insects and echinoderm GSS evolved independently from IGF and, thus, are not true orthologs, but the result of convergent evolution.

Ambulacrarian insulin-related peptides and their putative receptors suggest how insulin and similar peptides may have evolved from Insulin-like Growth Factor

Background: Insulin is evolutionarily related to the insulin-like growth factors (IGFs) and like the latter stimulates a receptor tyrosine kinase (RTK) that transfers the extracellular hormonal signal into an intracellular response. Other hormones related to insulin, such as relaxin, do not use an RTK, but a G-protein coupled receptor (GPCR). This is unusual since evolutionarily related hormones typically either use the same or paralogous receptors. In arthropods three different IGF-related peptides likely evolved from a gene triplication, as in several species genes coding these three peptides are located next to one another on the same chromosomal fragment. Of these three hormones one, an IGF-like hormone, acts through an RTK, while the other two use a GPCR. This suggests that the ancestral IGF-like peptide may have used both types of receptors. These arthropod insulin-like peptides have homologs in vertebrates, which suggests that the initial gene triplication was perhaps already present in the last common ancestor of deuterostomes and protostomes. It would be interesting to know whether this is indeed so and to establish how insulin and other insulin-like peptides might be related to this trio of IGF-related hormones. Methodology: Genes coding insulin and related peptides as well as their putative receptors were identified in genomes and transcriptomes from echinoderms and hemichordates. Results: A similar triplet of genes coding insulin-like peptides is also found in some hemichordates and echinoderms. Two of the three ambulacrarian peptides are orthologs of arthropod IGF and Drosophila insulin-like peptide 7 (dilp7), while the third one looks like an ortholog of the arthropod peptide gonadulin. In echinoderms two novel insulin-like peptides emerged, gonad stimulating substance (GSS) and multinsulin, likely from gene duplications of the IGF and dilp7-like genes respectively. However, no novel receptors for insulin-like peptides evolved. If IGF were to act through both a GPCR and an RTK it would suggest that GSS acts on only one of the two receptors, possibly the RTK. The evolution of GSS from IGF may represent a pattern, where IGF gene duplications lead to novel genes coding shorter peptides that have lost their ability to activate a GPCR. It is likely this is how insulin and the insect neuroendocrine insulin-like peptides evolved independently from IGF. Conclusion: The local gene triplication previously described from arthropods that yielded three genes coding IGF-related peptides was already present in the last common ancestor of protostomes and deuterostomes. It seems plausible that insulin and other insulin-like peptides, such as those produced by neuroendocrine cells in the brain of insects and echinoderm GSS evolved independently from IGF and thus are not true orthologs, but the result of convergent evolution.

Auxin: Hormonal Signal Required for Seed Development and Dormancy

The production of viable seeds is a key event in the life cycle of higher plants. Historically, abscisic acid (ABA) and gibberellin (GAs) were considered the main hormones that regulate seed formation. However, auxin has recently emerged as an essential player that modulates, in conjunction with ABA, different cellular processes involved in seed development as well as the induction, regulation and maintenance of primary dormancy (PD). This review examines and discusses the key role of auxin as a signaling molecule that coordinates seed life. The cellular machinery involved in the synthesis and transport of auxin, as well as their cellular and tissue compartmentalization, is crucial for the development of the endosperm and seed-coat. Thus, auxin is an essential compound involved in integuments development, and its transport from endosperm is regulated by AGAMOUS-LIKE62 (AGL62) whose transcript is specifically expressed in the endosperm. In addition, recent biochemical and genetic evidence supports the involvement of auxins in PD. In this process, the participation of the transcriptional regulator ABA INSENSITIVE3 (ABI3) is critical, revealing a cross-talk between auxin and ABA signaling. Future experimental aimed at advancing knowledge of the role of auxins in seed development and PD are also discussed.

Thyroid Hormone Action and Energy Expenditure

Energy metabolism is one of the most recognized targets of thyroid hormone action, which indeed plays a critical role in modulating energy expenditure in all of its components. This is because thyroid hormone receptors are ubiquitous, and thyroid hormones interact and influence most metabolic pathways in virtually all systems throughout the entire life of the organism. The pleiotropic actions of thyroid hormone are the results of interaction between the local availability of T3 and the signal transduction machinery, which confer in physiologic conditions time and tissue specificity of the hormonal signal despite negligible variations in circulating levels. Historically, the measurement of energy expenditure has been used as the gold standard for the clinical assessment of the hormonal action until the advent of the immunoassays for TSH and thyroid hormone, which have since been used as proxy for measurement of thyroid hormone action. Although the clinical correlates between thyroid hormone action and energy expenditure in cases of extreme dysfunction (florid hyperthyroidism or hypothyroidism) are well recognized, there is still controversy on the effects of moderate, subclinical thyroid dysfunction on energy expenditure and, ultimately, on body weight trajectory. Moreover, little information is available on the effects of thyroid hormone replacement therapy on energy expenditure. This mini review is aimed to define the clinical relevance of thyroid hormone action in normal physiology and functional disorders, as well the effects of thyroid hormone therapy on energy expenditure and the effects of changes in energy status on the thyroid hormone axis.

Central Interleukin-1βSuppresses the Nocturnal Secretion of Melatonin

In vertebrates, numerous processes occur in a rhythmic manner. The hormonal signal reliably reflecting the environmental light conditions is melatonin. Nocturnal melatonin secretion patterns could be disturbed in pathophysiological states, including inflammation, Alzheimer’s disease, and depression. All of these states share common elements in their aetiology, including the overexpression of interleukin- (IL-) 1βin the central nervous system. Therefore, the present study was designed to determine the effect of the central injection of exogenous IL-1βon melatonin release and on the expression of the enzymes of the melatonin biosynthetic pathway in the pineal gland of ewe. It was found that intracerebroventricular injections of IL-1β(50 µg/animal) suppressed(P<0.05)nocturnal melatonin secretion in sheep regardless of the photoperiod. This may have resulted from decreased(P<0.05)synthesis of the melatonin intermediate serotonin, which may have resulted, at least partially, from a reduced expression of tryptophan hydroxylase. IL-1βalso inhibited(P<0.05)the expression of the melatonin rhythm enzyme arylalkylamine-N-acetyltransferase and hydroxyindole-O-methyltransferase. However, the ability of IL-1βto affect the expression of these enzymes was dependent upon the photoperiod. Our study may shed new light on the role of central IL-1βin the aetiology of disruptions in melatonin secretion.