Microbial enhancement of plant nutrient acquisition

Nutrient availability is a determining factor for crop yield and quality. While fertilization is a major approach for improving plant nutrition, its efficacy can be limited and the production and application of fertilizers frequently bring problems to the environment. A large number of soil microbes are capable of enhancing plant nutrient acquisition and thereby offer environmentally benign solutions to meet the requirements of plant nutrition. Herein we provide summations of how beneficial microbes enhance plant acquisition of macronutrients and micronutrients. We also review recent studies on nutrition-dependent plant-microbe interactions, which highlight the plant’s initiative in establishing or deterring the plant-microbe association. By dissecting complex signaling interactions between microbes within the root microbiome, a greater understanding of microbe-enhanced plant nutrition under specific biotic and abiotic stresses will be possible.

Basic Protein Modules Combining Abscisic Acid and Light Signaling in Arabidopsis

It is generally accepted that plants use the complex signaling system regulated by light and abscisic acid (ABA) signaling components to optimize growth and development in different situations. The role of ABA–light interactions is evident in the coupling of stress defense reactions with seed germination and root development, maintaining of stem cell identity and stem cell specification, stem elongation and leaf development, flowering and fruit formation, senescence, and shade avoidance. All these processes are regulated jointly by the ABA–light signaling system. Although a lot of work has been devoted to ABA–light signal interactions, there is still no systematic description of central signaling components and protein modules, which jointly regulate plant development. New data have emerged to promote understanding of how ABA and light signals are integrated at the molecular level, representing an extensively growing area of research. This work is intended to fill existing gaps by using literature data combined with bioinformatics analysis.

miR-137 Inhibition of the Invasion, Metastasis, and Epithelial-Mesenchymal Transition of Nasopharyngeal Cancer by Regulating KDM1A

One of the most frequent malignancies in the head and neck is nasopharyngeal carcinoma (NPC). MicroRNAs, a kind of tiny noncoding RNA molecule, have been used as negative regulators in different types of cancer therapy in recent decades by downregulating their targets. Recent research suggests that microRNAs play an important role in cancer’s epithelial-to-mesenchymal transition (EMT), supporting or inhibiting EMT development. The epithelial-to-mesenchymal transition (EMT) is linked to a variety of cancer-related activities, including growth, metastasis, and invasion. Previous research has linked EMT to cancer stem-like characteristics as well as treatment resistance. Moreover, since microRNAs (miRNAs) are important regulators of the EMT phenotype, certain miRNAs have an effect on cancer stemness and treatment resistance. As a result, both fundamental research and clinical therapy benefit from knowing the connection between EMT-associated miRNAs and cancer stemness/drug resistance. As a result, we looked at the different functions that EMT-associated miRNAs (miR-137) play in the stem-like characteristics of malignant cells in this article. Then we looked at how EMT-associated miRNAs interact with nasopharyngeal cancer’s drug-resistant complex signaling pathways. Using qRT-PCR, we evaluated the performance of several micro RNAs with the proposed miR-137 for inhibiting invasion, metastasis, and the EMT process. In conclusion, our findings showed that miR-137 acted as a tumor suppressor gene in controlling NPC EMT and metastasis and that it may be a new therapeutic strategy and prognosis marker for the disease.

Formation and Development of Taproots in Deciduous Tree Species

Trees are generally long-lived and are therefore exposed to numerous episodes of external stimuli and adverse environmental conditions. In certain trees e.g., oaks, taproots evolved to increase the tree’s ability to acquire water from deeper soil layers. Despite the significant role of taproots, little is known about the growth regulation through internal factors (genes, phytohormones, and micro-RNAs), regulating taproot formation and growth, or the effect of external factors, e.g., drought. The interaction of internal and external stimuli, involving complex signaling pathways, regulates taproot growth during tip formation and the regulation of cell division in the root apical meristem (RAM). Assuming that the RAM is the primary regulatory center responsible for taproot growth, factors affecting the RAM function provide fundamental information on the mechanisms affecting taproot development.

Gliding motility of Plasmodium merozoites

Plasmodium malaria parasites are obligate intracellular protozoans that use a unique form of locomotion, termed gliding motility, to move through host tissues and invade cells. The process is substrate dependent and powered by an actomyosin motor that drives the posterior translocation of extracellular adhesins which, in turn, propel the parasite forward. Gliding motility is essential for tissue translocation in the sporozoite and ookinete stages; however, the short-lived erythrocyte-invading merozoite stage has never been observed to undergo gliding movement. Here we show Plasmodium merozoites possess the ability to undergo gliding motility in vitro and that this mechanism is likely an important precursor step for successful parasite invasion. We demonstrate that two human infective species, Plasmodium falciparum and Plasmodium knowlesi, have distinct merozoite motility profiles which may reflect distinct invasion strategies. Additionally, we develop and validate a higher throughput assay to evaluate the effects of genetic and pharmacological perturbations on both the molecular motor and the complex signaling cascade that regulates motility in merozoites. The discovery of merozoite motility provides a model to study the glideosome and adds a dimension for work aiming to develop treatments targeting the blood stage invasion pathways.

Reviewing cancer’s biology: an eclectic approach

Background Cancer refers to a group of some of the worldwide most diagnosed and deadliest pathophysiological conditions that conquered researchers’ attention for decades and yet begs for more questions for a full comprehension of its complex cellular and molecular pathology. Main body The disease conditions are commonly characterized by unrestricted cell proliferation and dysfunctional replicative senescence pathways. In fact, the cell cycle operates under the rigorous control of complex signaling pathways involving cyclins and cyclin-dependent kinases assumed to be specific to each phase of the cycle. At each of these checkpoints, the cell is checked essentially for its DNA integrity. Genetic defects observed in these molecules (i.e., cyclins, cyclin-dependent kinases) are common features of cancer cells. Nevertheless, each cancer is different concerning its molecular and cellular etiology. These could range from the genetic defects mechanisms and/or the environmental conditions favoring epigenetically harbored homeostasis driving tumorigenesis alongside with the intratumoral heterogeneity with respect to the model that the tumor follows. Conclusions This review is not meant to be an exhaustive interpretation of carcinogenesis but to summarize some basic features of the molecular etiology of cancer and the intratumoral heterogeneity models that eventually bolster anticancer drug resistance for a more efficient design of drug targeting the pitfalls of the models.

Hypothalamic endocannabinoids in obesity: an old story with new challenges

The crucial role of the hypothalamus in the pathogenesis of obesity is widely recognized, while the precise molecular and cellular mechanisms involved are the focus of intense research. A disrupted endocannabinoid system, which critically modulates feeding and metabolic functions, through central and peripheral mechanisms, is a landmark indicator of obesity, as corroborated by investigations centered on the cannabinoid receptor CB1, considered to offer promise in terms of pharmacologically targeted treatment for obesity. In recent years, novel insights have been obtained, not only into relation to the mode of action of CB receptors, but also CB ligands, non-CB receptors, and metabolizing enzymes considered to be part of the endocannabinoid system (particularly the hypothalamus). The outcome has been a substantial expansion in knowledge of this complex signaling system and in drug development. Here we review recent literature, providing further evidence on the role of hypothalamic endocannabinoids in regulating energy balance and the implication for the pathophysiology of obesity. We discuss how these lipids are dynamically regulated in obesity onset, by diet and metabolic hormones in specific hypothalamic neurons, the impact of gender, and the role of endocannabinoid metabolizing enzymes as promising targets for tackling obesity and related diseases.

mTORC1 Crosstalk With Stress Granules in Aging and Age-Related Diseases

The mechanistic target of rapamycin complex 1 (mTORC1) kinase is a master regulator of metabolism and aging. A complex signaling network converges on mTORC1 and integrates growth factor, nutrient and stress signals. Aging is a dynamic process characterized by declining cellular survival, renewal, and fertility. Stressors elicited by aging hallmarks such as mitochondrial malfunction, loss of proteostasis, genomic instability and telomere shortening impinge on mTORC1 thereby contributing to age-related processes. Stress granules (SGs) constitute a cytoplasmic non-membranous compartment formed by RNA-protein aggregates, which control RNA metabolism, signaling, and survival under stress. Increasing evidence reveals complex crosstalk between the mTORC1 network and SGs. In this review, we cover stressors elicited by aging hallmarks that impinge on mTORC1 and SGs. We discuss their interplay, and we highlight possible links in the context of aging and age-related diseases.

Cell death leaves a new TRAIL

Cell death involves numerous mechanisms that can be cross-regulated through a complex signaling network. In this issue, Bozkurt et al. (2021. J. Cell Biol.https://doi.org/10.1083/jcb.202010030) identify a new connection in the network: signaling from TRAIL, a canonical inducer of apoptosis, can also induce a form of cell death called entosis, which has implications for cancer progression.

Particulate Matter Exposure and Allergic Rhinitis: The Role of Plasmatic Extracellular Vesicles and Bacterial Nasal Microbiome

Particulate matter (PM) exposure is linked to the worsening of respiratory conditions, including allergic rhinitis (AR), as it can trigger nasal and systemic inflammation. To unveil the underlying molecular mechanisms, we investigated the effects of PM exposure on the release of plasmatic extracellular vesicles (EV) and on the complex cross-talk between the host and the nasal microbiome. To this aim, we evaluated the effects of PM10 and PM2.5 exposures on both the bacteria-derived-EV portion (bEV) and the host-derived EVs (hEV), as well as on bacterial nasal microbiome (bNM) features in 26 AR patients and 24 matched healthy subjects (HS). In addition, we assessed the role exerted by the bNM as a modifier of PM effects on the complex EV signaling network in the paradigmatic context of AR. We observed that PM exposure differently affected EV release and bNM composition in HS compared to AR, thus potentially contributing to the molecular mechanisms underlying AR. The obtained results represent the first step towards the understanding of the complex signaling network linking external stimuli, bNM composition, and the immune risponse.