Managing Micronutrients for Improving Soil Fertility, Health, and Soybean Yield

Plants need only a small quantity of micronutrients, but they are essential for vital cell functions. Critical micronutrients for plant growth and development include iron (Fe), boron (B), manganese (Mn), zinc (Zn), copper (Cu), molybdenum (Mo), chlorine (Cl), and nickel (Ni). The deficiency of one or more micronutrients can greatly affect plant production and quality. To explore the potential for using micronutrients, we reviewed the literature evaluating the effect of micronutrients on soybean production in the U.S. Midwest and beyond. Soil and foliar applications were the major micronutrient application methods. Overall, studies indicated the positive yield response of soybean to micronutrients. However, soybean yield response to micronutrients was not consistent among studies, mainly because of different environmental conditions such as soil type, soil organic matter (SOM), moisture, and temperature. Despite this inconsistency, there has been increased pressure for growers to apply micronutrients to soybeans due to a fact that deficiencies have increased with the increased use of high-yielding cultivars. Further studies on quantification and variable rate application of micronutrients under different soil and environmental conditions are warranted to acquire more knowledge and improve the micronutrient management strategies in soybean. Since the SOM could meet the micronutrient need of many crops, management strategies that increase SOM should be encouraged to ensure nutrient availability and improve soil fertility and health for sustainable soybean production.

Exogenous Hydrogen Sulfide Plays an Important Role by Regulating Autophagy in Diabetic-Related Diseases

Autophagy is a vital cell mechanism which plays an important role in many physiological processes including clearing long-lived, accumulated and misfolded proteins, removing damaged organelles and regulating growth and aging. Autophagy also participates in a variety of biological functions, such as development, cell differentiation, resistance to pathogens and nutritional hunger. Recently, autophagy has been reported to be involved in diabetes, but the mechanism is not fully understood. Hydrogen sulfide (H2S) is a colorless, water-soluble, flammable gas with the typical odor of rotten eggs, which has been known as a highly toxic gas for many years. However, it has been reported recently that H2S, together with nitric oxide and carbon monoxide, is an important gas signal transduction molecule. H2S has been reported to play a protective role in many diabetes-related diseases, but the mechanism is not fully clear. Recent studies indicate that H2S plays an important role by regulating autophagy in many diseases including cancer, tissue fibrosis diseases and glycometabolic diseases; however, the related mechanism has not been fully studied. In this review, we summarize recent research on the role of H2S in regulating autophagy in diabetic-related diseases to provide references for future related research.

Crosstalk between H2A variant-specific modifications impacts vital cell functions

Selection of C-terminal motifs participated in evolution of distinct histone H2A variants. Hybrid types of variants combining motifs from distinct H2A classes are extremely rare. This suggests that the proximity between the motif cases interferes with their function. We studied this question in flowering plants that evolved sporadically a hybrid H2A variant combining the SQ motif of H2A.X that participates in the DNA damage response with the KSPK motif of H2A.W that stabilizes heterochromatin. Our inventory of PTMs of H2A.W variants showed that in vivo the cell cycle-dependent kinase CDKA phosphorylates the KSPK motif of H2A.W but only in absence of an SQ motif. Phosphomimicry of KSPK prevented DNA damage response by the SQ motif of the hybrid H2A.W/X variant. In a synthetic yeast expressing the hybrid H2A.W/X variant, phosphorylation of KSPK prevented binding of the BRCT-domain protein Mdb1 to phosphorylated SQ and impaired response to DNA damage. Our findings illustrate that PTMs mediate interference between the function of H2A variant specific C-terminal motifs. Such interference could explain the mutual exclusion of motifs that led to evolution of H2A variants.

High Value Phycotoxins From the Dinoflagellate Prorocentrum

Marine dinoflagellates produce chemically diverse compounds, with a wide range of biological activity (antimicrobial, anticancer, treatment of neurodegenerative disease along with use as biomedical research tools). Chemical diversity is highlighted by their production of molecules such as the saxitoxin family of alkaloids (C10H17N7O4 – 299 g/mol) to the amphipathic maitotoxin (C164H256O68S2Na2 – 3,422 g/mol), representing one of the largest and most complex secondary metabolites characterized. Dinoflagellates, are most well-known for the production of red tides which are frequently toxic, including okadaic acid and related dinophysistoxins, which are tumor promoters. The mode of action for these phycotoxins, is by specific inhibition of protein phosphatases, enzymes essential in regulation of many cellular processes. Hence, these compounds are being used for vital cell regulation studies. However, the availability of useful amounts of these compounds has restricted research. Chemical synthesis of some compounds such as okadaic acid has been investigated, but the complexity of the molecule resulted in many lengthy steps and achieved only a poor yield. The use of naturally occurring phytoplankton has been investigated as a potential source of these compounds, but it has been shown to be unreliable and impractical. The most practical option is large scale culture with down-stream processing/purification which requires specialist facilities and expertise. This review, describes the biotechnological potential of these organisms and the challenges to achieve useful yields of high quality phycotoxins using Prorocentrum spp. as an example to produce okadaic acid.

Cytokine Secretions in Partial Breast Tumor Microenvironment With and Without Sulforaphane

Objectives Triple-negative breast cancer (TNBC) comprises 10–20% of breast cancer cases. It is particularly aggressive with limited and deleterious treatment options. Increasingly, research confirms that communication between cancer cells and neighboring macrophages promotes disease progression in part by secretion of cytokines that increase tumor cell proliferation, invasion, and metastasis. Sulforaphane (SFN) is a chemopreventive phytochemical found in cruciferous vegetables (broccoli) shown to alter cytokine secretion in macrophages and breast cancer cells grown in single culture. However, its effect in the tumor microenvironment remains unclear. This study aims to characterize cytokine profiles in media where TNBC cells and macrophages are grown in coculture with and without SFN treatment. We expect SFN to modify cytokine secretions in coculture media, suggesting SFN may disrupt vital cell-cell signaling needed for cancer progression. Methods TNBC cells (MDA-MB-231) were grown in Transwell plates with and without macrophages (THP-1 cells differentiated with PMA). Cell cultures (n = 3) were treated with either 15 μM SFN, DMSO (vehicle-control), or a non-treatment control. Cytokine levels were evaluated in media at 24 and 48 hours after treatment using BioPlex 2000 assay. Results Treatment with sulforaphane significantly reduced the levels of several targets in coculture including IL-1ra, IL-4, IL-5, IL-10, IL-12, IL-13, IL-15, IL-17, CCL2 (MCP-1), CCL11, CCL22, CCL26, CXCL12, IFN-y, G-CSF, GM-CSF, Eotaxin, and VEGF. Conversely, MIF was elevated following treatment. Effects were discovered at 24-hour and 48-hour time points. Conclusions We demonstrated that SFN altered the levels of numerous cellular signaling proteins in cancer cell-macrophage coculture, many of which are known to be involved with breast cancer progression. These results reveal mechanistic links underlying SFNs chemopreventive function and bolster SFNs potential as a treatment strategy for TNBC. Funding Sources Department of Nutrition and Food Science, CSU Chico; Graduate Studies, CSU Chico; CSUPERB: CSU Program for Education and Research in Biotechnology.

MASA PANDEMI COVID-19 SEBAGAI “SEKOLAH KEMANUSIAAN” BAGI KELUARGA KRISTIANI

The family is a domestic ecclesia that is called to cultivate seeds of faith and joyful love for its members and for other families. As ecclesia domestica, families need to be aware of their unique calling in the midst of the complex challenges faced today, namely to become a sign of real love in the life of the world. The family becomes the first and vital cell for society and a deeper humanitarian school. The Covid-19 pandemic period can be an opportunity to turn families into humanitarian schools, where human values ​​grow and develop, a house of holiness, where the virtues of the gospel grow, and the community of mercy is in accordance with the ideals of Christian marriage. The period of the Covid-19 pandemic should be a momentum for reflection to increase family dialogue, harmony, and assistance for children.

New twists in actin–microtubule interactions

Actin filaments and microtubules are cytoskeletal polymers that participate in many vital cell functions including division, morphogenesis, phagocytosis, and motility. Despite the persistent dogma that actin filament and microtubule networks are distinct in localization, structure, and function, a growing body of evidence shows that these elements are choreographed through intricate mechanisms sensitive to either polymer. Many proteins and cellular signals that mediate actin–microtubule interactions have already been identified. However, the impact of these regulators is typically assessed with actin filament or microtubule polymers alone, independent of the other system. Further, unconventional modes and regulators coordinating actin–microtubule interactions are still being discovered. Here we examine several methods of actin–microtubule crosstalk with an emphasis on the molecular links between both polymer systems and their higher-order interactions.

COVID-19 and Immune Function – “A Significant” Zinc

The pandemic COVID-19 is the most terrible calamity of the present human history also it has led to the worldwide issue of public health as a primary health safety problem. It was assumed that the infection of COVID -19 has two-phases, the immune protective as well as damaging phase. In the immune protective phase, clinicians try to enhance the patient immune response, and in the immune damaging phase, clinicians try to control the inflammatory immune response. Zinc belongs to the d-block or a transition element, it is an indispensable trace metal needed for vital cell activities like growth, as well as cell survival. It has significant contributions to immune homeostasis and functions; zinc inadequacy reduces primary and secondary immune responses equally. Studies have shown people who are deficient in zinc are more susceptible to infection. An inclusive knowledge of the bioavailability of the transition metal Zinc will help to be aware of those that are valuable and protective for the population's health. This work is concentrated on the significance of Zinc for the immune function, the presence of it’s in optimum amounts, and how it is beneficial to health in general and in fighting with COVID 19 in particular until today.

An Insight Into Mitochondrial Dysfunction and its Implications in Neuro-logical Diseases

Abstract:: In the last few years, a massive increase in the research has been observed that focusses on investigating the role of mitochondria in pathogenesis of several neurodegenerative disorders. Mitochondria are vital cell organelles having im-portant roles in different cellular processes including energy production, calcium signaling, ROS generation, apoptosis, etc. Therefore, healthy mitochondria are necessary for cell survival and functioning. It would seem feasible that mitochondrial dysfunction will have implications in various pathological conditions. A large body of evidence indicates the role of mito-chondrion as a potential key player in the loss or dysfunction of neurons in various neurodegenerative disorders. In this review, we provide an insight into the mitochondrial dysfunction and its involvement in the pathology of several neurolog-ical diseases such as Alzheimer’s disease, Parkinson’s disease, Amyotrophic Lateral Sclerosis, Hypoxic-Ischemic Brain Injury and many more.