Review Paper on Effect of Micronutrients for Crop Production

Micronutrients are essentially as important as macronutrients to have better growth, yield and quality in plants. There requirement by plants is in trace amounts. Boron, iron, copper, zinc, manganese, magnesium and molybdenum constitute main micronutrients required by different crops in variable quantities. The requirement of micronutrients is partly met from the soil or through chemical fertilizer or through other sources. Various physical and metabolic functions are governed by these mineral nutrients. Boron is particularly essential in pollen germination, copper plays major role in photosynthesis and increases sugar content in fruits, chlorophyll synthesis and phosphorus availability is enhanced by manganese, iron acts as an oxygen carrier and promotes chlorophyll formation, while, zinc aids plant growth hormones and enzyme system. Yield and quality of agricultural products increased with micronutrients application, therefore human and animal health is protected with feed of enrichment plant materials. Each essential element only when can perform its role in plant nutrition properly that other necessary elements are available in balanced ratios for plant. therefore in the plant manganese plays an important role on oxidation and reduction processes, as electron transport in photosynthesis. Manganese deficiency has very serious effects on non-structural carbohydrates, and roots carbohydrates especially. Crops quality and quantity decreased due to manganese deficiency, and this is due to low fertility of pollen and low in carbohydrates during grain filling. In the xylem routes zinc is transmitted to divalent form or with organic acids bond. In the phloem sap zinc makes up complex with organic acids with low molecular weight, and increases its concentration. Zinc deficiency can be seen in eroded, calcareous and weathering acidic soils. Zinc deficiency is often accompanied with iron deficiency in calcareous soils. Iron in the soil is the fourth abundant element on earth, but its amount was low or not available for the plants and microorganisms needs, due to low solubility of minerals containing iron in many places the world, especially in arid region with alkaline soils.

Key Plant, Key Pests: Sago Palm (Cycas revoluta)

This series of Key Plant, Key Pests publications are designed for Florida gardeners, horticulturalists, and landscape professionals to help identify common pests associated with common Florida flora. This new 4-page publication of the UF/IFAS Environmental Horticulture Department provides information and general management recommendations for aulacaspis scale, other scales, mealybugs, and manganese deficiency. https://edis.ifas.ufl.edu/ep608

Generation of a Polyclonal Antibody against the Mouse Metal Transporter ZIP8

ZIP8 is a newly identified metal transporter. In human patients, mutations in ZIP8 result in severe manganese deficiency, suggesting a critical role for ZIP8 in regulating systemic manganese homeostasis. In mice, the deletion of ZIP8 recapitulates the symptoms of patients with ZIP8 mutations. However, further studies using mouse models to examine ZIP8′s function were hindered by the lack of suitable antibodies to detect endogenous ZIP8 protein. In this study, we report the design, generation, and validation of a polyclonal antibody against mouse ZIP8. We have demonstrated that the newly generated antibody can be reliably used in immunoblotting analysis to detect endogenous ZIP8 protein in mouse tissues. The successful generation and validation of anti-mouse ZIP8 antibody provide opportunities to further examine the function and regulation of this metal transporter. In addition, our study may provide valuable insights into the future development of antibodies targeting polytopic membrane proteins.

Changes in protein and mineral metabolism in broiler chickens with perosis

Perosis is one of the most common leg pathologies in broiler chickens, during the period of intense weight gain – at the age of 14–35 days. Due to manganese deficiency, the number of sick birds can reach up to 5% of the flock. These studies were carried out in order to establish changes in some indicators of protein, macro- and micromineral metabolism in the blood serum of clinically healthy broiler chickens and birds with perosis at 14, 21 and 28 days of age. A batch of 2,000 Cobb-500 crossbred broiler chickens was selected. Two groups of chickens were directly involved in the research, in which blood was taken at the age of 14, 21 and 28 days: healthy birds and those with perosis signs. Clinical studies showed that 8.0% of chickens on 28th day suffered from perosis. Trace mineral biochemical parameters of serum and blood of broiler chickens with perosis on the 28th day of life significantly differed from those of healthy birds (manganese and zinc). It was found that on the 28th day of life the weight of chickens with perosis was reduced by 42.7%, causing a loss of weight 88 kg per batch of 2000 birds, with a consumption of feed 140 kg. The obtained data will allow the development of early perosis prevention schemes in broiler chickens, which will help manage production losses and increase its profitability. On farms, to prevent the occurrence of perosis, it is necessary to take into account the technological factors of the production of compound feed. Also, an increase in the level of total protein and albumin in serum in the blood may indicate inflammatory processes and dehydration of the body. Therefore, it is better to site a sick bird separately for rearing or hand over to a sanitary culling.

Loss of slc39a14 causes simultaneous manganese deficiency and hypersensitivity in zebrafish

Mutations in SLC39A14, a manganese uptake transporter, lead to a neurodegenerative disorder characterised by accumulation of manganese in the brain and rapidly progressive dystonia-parkinsonism (Hypermanganesemia with Dystonia 2, HMNDYT2). Similar to the human phenotype, zebrafish slc39a14U801-/- mutants show prominent brain manganese accumulation and abnormal locomotor behaviour. In order to identify novel potential targets of manganese neurotoxicity, we performed transcriptome analysis of individual homozygous mutant and sibling slc39a14U801 zebrafish at five days post fertilisation unexposed and exposed to MnCl2. Anatomical gene enrichment analysis confirmed that differentially expressed genes map to the central nervous system and eye. Biological interpretation of differentially expressed genes suggests that calcium dyshomeostasis, activation of the unfolded protein response, oxidative stress, mitochondrial dysfunction, lysosomal disruption, apoptosis and autophagy, and interference with proteostasis are key events in manganese neurotoxicity. Differential expression of visual phototransduction genes also predicted visual dysfunction in mutant larvae which was confirmed by the absence of visual background adaptation and a diminished optokinetic reflex. Surprisingly, we found a group of differentially expressed genes in mutant larvae that normalised upon MnCl2 treatment suggesting that, in addition to neurotoxicity, manganese deficiency is present either subcellularly or in specific cells or tissues. This may have important implications for treatment as manganese chelation may aggravate neurological symptoms. Our analyses show that slc39a14U801-/- mutant zebrafish present a powerful model to study the cellular and molecular mechanisms underlying disrupted manganese homeostasis.Significance statementManganese neurotoxicity leading to progressive dystonia-parkinsonism is a characteristic feature of Hypermanganesemia with dystonia 2 (HMNDYT2) caused by mutations in SLC39A14, a manganese uptake transporter. Transcriptional profiling in slc39a14U801 loss-of-function zebrafish suggests that, in addition to manganese neurotoxicity, subcellular or cell type specific manganese deficiency contributes to the disease phenotype. Both manganese overload and deficiency appear to be associated with Ca2+ dyshomeostasis. We further demonstrate that activation of the unfolded protein response, oxidative stress, mitochondrial dysfunction, apoptosis and autophagy, and disrupted proteostasis are likely downstream events in manganese neurotoxicity. Our study shows that the zebrafish slc39a14U801 loss-of-function mutant is a powerful model to elucidate the mechanistic basis of diseases affected by manganese dyshomeostasis.