Shedding light on shade: ecological perspectives of understorey plant life

Shade, in ecological sense, is not merely a lack of light, but a multi-faceted phenomenon that creates new and complex settings for community and ecosystem dynamics. Tolerating shade therefore affects plants’ ability to cope with other stressors, and also shape its interactions with surrounding organisms. The aim of this broad review was to map our current knowledge about how shade affects plants, plant communities and ecosystems – to gather together knowledge of what we know, but also to point out what we do not yet know. This review covers the following topics: the nature of shade, and ecological and physiological complexities related to growing under a canopy; plants’ capability of tolerating other stress factors while living under a shade – resource trade-offs and polytolerance of abiotic stress; ontogenetic effects of shade tolerance; coexistence patterns under the canopy – how shade determines the forest structure and diversity; shade-induced abiotic dynamics in understorey vegetation, including changing patterns of irradiance, temperature and humidity under the canopy; shade-driven plant–plant and plant–animal interactions – how shade mediates facilitation and stress, and how it creates differentiated environment for different herbivores and pollinators, including the role of volatile organic compounds. We also discuss the ways how vegetation in understorey environments will be affected by climate change, as shade might play a significant role in mitigating negative effects of climate change. Our review shows that living under a shade affects biotic and abiotic stress tolerance of plants, it also influences the outcomes of both symbiotic and competitive plant–plant and plant–animal interactions in a complex and dynamic manner. The current knowledge of shade-related mechanisms is rather ample, however there is much room for progress in integrating different implications of the multifaceted nature of shade into consistent and integral understanding how communities and ecosystems function.     

Shedding light on large-scale chromatin reorganization in Arabidopsis thaliana

Plants need to respond quickly and appropriately to various types of light signals from the environment to optimize growth and development. The immediate response to shading, reduced photon flux (low light), and changes in spectral quality involves changes in gene regulation. In the case of more persistent shade, the plant shows a dramatic change in the organization of chromatin. Both plant responses are controlled via photoreceptor signaling proteins. Recently, several studies have revealed similar features of chromatin reorganization in response to various abiotic and biotic signals, while others have unveiled intricate molecular networks of light signaling towards gene regulation. This opinion paper briefly describes the chromatin (de)compaction response from a light-signaling perspective to provide a link between chromatin and the molecular network of photoreceptors and E3 ubiquitin ligase complexes.     

Shedding light on melanoma

Not just confined to sunny places, the incidence of melanoma has been rising in all fair-skinned populations around the world. How much is known about the causes of this disease, and can this knowledge be applied to preventive strategies?     

Shedding a little light on light chains

Myosin II regulatory light chains have an important role in the organization and function of the contractile machinery at cytokinesis. Two recent reports provide new insights into these important proteins.     

Shedding light on ADAM metalloproteinases

ADAM metalloproteinase disintegrins have emerged as the major proteinase family that mediates ectodomain shedding, the proteolytic release of extracellular domains from their membrane-bound precursors. Recent gene-manipulation studies have established the role of ADAM-mediated shedding in mammalian physiology and, in addition, raised the issue of functional redundancy among ADAM sheddases. ADAM sheddases activate, for example, growth factors and cytokines, thus regulating signalling pathways that are important in development and pathological processes such as cancer. The recent studies have also begun to elucidate the substrate specificity and the mechanisms that control ADAM-mediated shedding events that regulate, for example, growth-factor and Notch signalling, and the processing of the amyloid precursor protein.     

Shedding light on Merlin's wizardry

Inactivation of the tumor suppressor Merlin, encoded by the NF2 (Neurofibromatosis type 2) gene, contributes to malignant conversion in many cell types. Merlin is an Ezrin-Radixin-Moesin protein and localizes underneath the plasma membrane at cell-cell junctions and other actin-rich sites. Recent studies indicate that Merlin mediates contact inhibition of proliferation by blocking recruitment of Rac to the plasma membrane. In mitogen-stimulated cells, p21-activated kinase phosphorylates Ser518 in the C-terminus of Merlin, inactivating the growth suppressive function of the protein. Furthermore, the myosin phosphatase MYPT1-PP1delta, has been identified as a direct activator of Merlin and its inhibition has been linked to malignant transformation. Finally, studies in the fruit fly Drosophila melanogaster have revealed that Merlin functions together with the band 4.1 protein Expanded to promote [corrected] the endocytosis of many signaling receptors, limiting [corrected] their accumulation at the plasma membrane, and to activate [corrected] the Hippo signaling pathway. Here, we review these recent findings and their relevance to the tumor suppressor function of Merlin.     

Shedding light on prion disease

Several fatal, progressive neurodegenerative diseases, including various prion and prion-like disorders, are connected with the misfolding of specific proteins. These proteins misfold into toxic oligomeric species and a spectrum of distinct self-templating amyloid structures, termed strains. Hence, small molecules that prevent or reverse these protein-misfolding events might have therapeutic utility. Yet it is unclear whether a single small molecule can antagonize the complete repertoire of misfolded forms encompassing diverse amyloid polymorphs and soluble oligomers. We have begun to investigate this issue using the yeast prion protein, Sup35, as an experimental paradigm. We have discovered that a polyphenol, (-)epigallocatechin-3-gallate (EGCG), effectively inhibited the formation of infectious amyloid forms (prions) of Sup35 and even remodeled preassembled prions. Surprisingly, EGCG selectively modulated specific prion strains and even selected for EGCG-resistant prion strains with novel structural and biological characteristics. Thus, treatment with a single small molecule antagonist of amyloidogenesis can select for novel, drug-resistant amyloid polymorphs. Importantly, combining EGCG with another small molecule, 4,5-bis-(4-methoxyanilino)phthalimide, synergistically antagonized and remodeled a wide array of Sup35 prion strains without producing any drug-resistant prions. We suggest that minimal drug cocktails, small collections of drugs that collectively antagonize all amyloid polymorphs, should be identified to besiege various neurodegenerative disorders.