Exotic Prosopis juliflora suppresses understory diversity and promotes agricultural weeds more than a native congener

Plant Ecology - Exotic invasive plant species alter ecosystems and locally extirpate native plant species, and by doing so alter community structure. Changes in community structure may be...     

Pharmacological strategies for the regulation of inducible nitric oxide synthase: neurodegenerative versus neuroprotective mechanisms

Inducible nitric oxide synthase (iNOS) is one of three NOS isoforms generating nitric oxide (NO) by the conversion of l-arginine to l-citrulline. iNOS has been found to be a major contributor to initiation/exacerbation of the central nervous system (CNS) inflammatory/degenerative conditions through the production of excessive NO which generates reactive nitrogen species (RNSs). Activation of iNOS and NO generation has come to be accepted as a marker and therapeutic target in neuroinflammatory conditions such as those observed in ischemia, multiple sclerosis (MS), spinal cord injury (SCI), Alzheimer's disease (AD), and inherited peroxisomal (e.g. X-linked adrenoleukodystrophy; X-ALD) and lysosomal disorders (e.g. Krabbe's disease). However, with the emergence of reports on the neuroprotective facets of NO, the prior dogma about NO being solely detrimental has had to be modified. While RNSs such as peroxynitrite (ONOO(-)) have been linked to lipid peroxidation, neuronal/oligodendrocyte loss, and demyelination in neurodegenerative diseases, limited NO generation by GSNO has been found to promote vasodilation and attenuate vascular injury under the same ischemic conditions. NO generated from GSNO acts as second messenger molecular which through S-nitrosylation has been shown to control important cellular processes by regulation of expression/activity of certain proteins such as NF-kappaB. It is now believed that the environment and the context in which NO is produced largely determines the actions (good or bad) of this molecule. These multi-faceted aspects of NO make therapeutic interference with iNOS activity even more complicated since complete ablation of iNOS activity has been found to be rather more detrimental than protective in most neurodegenerative conditions. Investigators in search of iNOS modulating pharmacological agents have realized the need of a delicate balance so as to allow the production of physiologically relevant amounts of NO (such as those required for host defence/neutotransmission/vasodilation, etc.) but at the same time block the generation of RNSs through repressing excessive NO levels (such as those causing neuronal/tissue damage and demyelination, etc.). The past years have seen a noteworthy increase in novel agents that might prove useful in achieving the aim of harnessing the good and blocking the undesirable actions of NO. It is the aim of this review to provide basic insights into the NOS family of enzymes with special emphasis of the role of iNOS in the CNS, in the first part. In the second part of the review, we will strive to provide an exhaustive compilation of the prevalent strategies being tested for the therapeutic modulation of iNOS and NO production.     

Use of silenced plants in allelopathy bioassays: a novel approach

Volatile phytohormones or other chemicals can affect processes in distal plant parts but may also influence neighboring plants, and thereby function allelopathically. While this hypothesis has been widely discussed, rigorous tests are lacking. Transgenic plants, silenced in the production of an emitted chemical, are ideal tools to test the hypothesis that the release of a chemical can negatively influence the growth of neighbors (allelopathy). We used isogenic wild type (WT) and genetically transformed plants that lacked the ability to produce ethylene (ir-aco), as both “emitters” and “receivers” of this volatile phytohormone in experiments where receiver plants were only exposed to the headspace of WT or ir-aco emitters, in order to evaluate if natural ethylene releases can function allelopathically. Root growth (a proxy of plant fitness) of WT receivers correlated negatively with the number of WT emitters and headspace ethylene concentrations. Reducing ethylene concentrations in the headspace with the ethylene scrubber, KMnO₄, and using ir-aco seedlings as emitters restored root growth of WT receiver seedlings. 1-Aminocyclopropane-1-carboxylic acid (ethylene biosynthesis substrate) supplementation to WT but not ir-aco emitters inhibited root growth of ir-aco, but not WT receivers, suggesting increased sensitivity to exogenous ethylene of ir-aco seedlings. We conclude that plants genetically silenced in the production of a putative allelochemical are useful in determining if the emitted chemical functions allelopathically. Electronic supplementary material  The online version of this article (doi:) contains supplementary material, which is available to authorized users.     

Increased Plp1 gene expression leads to massive microglial cell activation and inflammation throughout the brain

PMD (Pelizaeus–Merzbacher disease) is a rare neurodegenerative disorder that impairs motor and cognitive functions and is associated with a shortened lifespan. The cause of PMD is mutations of the PLP1 [proteolipid protein 1 gene (human)] gene. Transgenic mice with increased Plp1 [proteolipid protein 1 gene (non-human)] copy number model most aspects of PMD patients with duplications. Hypomyelination and demyelination are believed to cause the neurological abnormalities in mammals with PLP1 duplications. We show, for the first time, intense microglial reactivity throughout the grey and white matter of a transgenic mouse line with increased copy number of the native Plp1 gene. Activated microglia in the white and grey matter of transgenic mice are found as early as postnatal day 7, before myelin commences in normal cerebra. This finding indicates that degeneration of myelin does not cause the microglial response. Microglial numbers are doubled due to in situ proliferation. Compared with the jp (jimpy) mouse, which has much more oligodendrocyte death and hardly any myelin, microglia in the overexpressors show a more dramatic microglial reactivity than jp, especially in the grey matter. Predictably, many classical markers of an inflammatory response, including TNF-α (tumour necrosis factor-α) and IL-6, are significantly up-regulated manyfold. Because inflammation is believed to contribute to axonal degeneration in multiple sclerosis and other neurodegenerative diseases, inflammation in mammals with increased Plp1 gene dosage may also contribute to axonal degeneration described in patients and rodents with PLP1 increased gene dosage.     

Interaction of 8-Hydroxyquinoline with Soil Environment Mediates Its Ecological Function

Background

Allelopathic functions of plant-released chemicals are often studied through growth bioassays assuming that these chemicals will directly impact plant growth. This overlooks the role of soil factors in mediating allelopathic activities of chemicals, particularly non-volatiles. Here we examined the allelopathic potential of 8-hydroxyquinoline (HQ), a chemical reported to be exuded from the roots of Centaurea diffusa.

Methodology/Principal Findings

Growth bioassays and HQ recovery experiments were performed in HQ-treated soils (non-sterile, sterile, organic matter-enriched and glucose-amended) and untreated control soil. Root growth of either Brassica campestris or Phalaris minor was not affected in HQ-treated non-sterile soil. Soil modifications (organic matter and glucose amendments) could not enhance the recovery of HQ in soil, which further supports the observation that HQ is not likely to be an allelopathic compound. Hydroxyquinoline-treated soil had lower values for the CO₂ release compared to untreated non-sterile soil. Soil sterilization significantly influenced the organic matter content, PO₄-P and total organic nitrogen levels.

Conclusion/Significance

Here, we concluded that evaluation of the effect of a chemical on plant growth is not enough in evaluating the ecological role of a chemical in plant-plant interactions. Interaction of the chemical with soil factors largely determines the impact of HQ on plant growth.     

Ecophysiological aspects of allelopathy

Allelochemicals play an important role in explaining plant growth inhibition in interspecies interactions and in structuring the plant community. Five aspects of allelochemicals are discussed from an ecophysiological perspective: (i) biosynthesis, (ii) mode of release, (iii) mode of action, (iv) detoxification and prevention of autotoxicity, and (v) joint action of allelochemicals. A discussion on identifying a compound as an allelochemical is also presented.