Plant Growth Promoting Rhizobacteria\u27s (PGPRS) Enzyme Dynamics in Soil Remediation

Soil is the basis of agriculture and consists of organic matters, minerals, water, and several gasses. All plants require soil both as an anchor to attach and as water and nutrient source. Unfortunately, lifestyles of humans, industrial progress, chemicals used in agriculture contaminate soil and cause soil pollution. A pollutant may be natural or human‐made in origin such as petroleum hydrocarbons, pesticides, heavy metals, and solvents. Since the quality of the soil affects the growth and product yield of plants, soil pollution is a crucial problem needs to be addressed urgently. Plant growth promoting rhizobacteria (PGPR) are microorganisms living in soil, on the plants roots, or inside the plant. PGPRs synthesize chemicals to stimulate plant growth and promote nutrient uptake, help degrading soil pollutants and fending off pathogens. While some pollutants can be degraded by enzymes produced by bacteria and fungi, degradation of heavy metals requires alternative methods. In this chapter, three enzymes produced by PGPRs are reviewed briefly. Aminocyclopropane‐1‐carboxylate (ACC) deaminase is responsible of lowering the ethylene levels of plants during stress conditions, whereas nitrogenase is responsible for N2 reduction to NH3. Moreover, phytase enables the degradation of phytate which is a main storage form of phosphate in plants

Making Soil More Accessible to Plants: The Case of Plant Growth Promoting Rhizobacteria

Plant Growth Promoting Rhizobacteria (PGPR) are beneficial soil bacteria that can live either symbiotically with plants at rhizosphere or as endophytes living on or inside of the host plants. There are two main mechanisms via PGPR contribute to the plant growth. Direct mechanism consists of phytohormone production (i.e. auxins (IAA), cytokinins and gibberellins), biological nitrogen fixation, solubilizing inorganic phosphates, mineralizing organic phosphate and producing organic matter such as amino acids. As indirect mechanisms, PGPR aid plants in combat against the pathogen microorganisms by means of stimulating the disease-resistance mechanism of plants, promote favorable symbiosis, decontaminate the soil of xenobiotics. PGPR can also help plants to cope against abiotic stress by lowering ethylene levels, or against pathogenic microorganism by means of secreting antibacterial/antifungal substances. Exact mechanisms of PGPR characteristics which stimulate the plant growth or product formation are still under investigation, yet in agriculture, PGPR are used as environmental friendly biofertilizers, biocontrol agents or biostimulants. These beneficial bacteria are usually introduced to the plants either in powder or liquid form or the seeds are covered with the inoculants before sowing. Plants are subject to many different environmental elements. Abiotic factors such as drought or water stress have been one of the main plant growth limiting factors. Agricultural PGPR application is an alternative solution against loss due to the environmental stresses, since breeding a plant with stress resistance trait is a very long and tricky process due to the fact that such traits are controlled by multiple genes. PGPR phytohormone and enzyme (i.e. ACC deaminase) production can decrease the stress levels of plants while enhancing the root structures

An investigation of the etiology and follow-up findings in 35 children with overgrowth syndromes, including biallelic SUZ12 variant.

Overgrowth-intellectual disability (OGID) syndromes are clinically and genetically heterogeneous group of disorders. The aim of this study was to examine the molecular etiology and long-term follow-up findings of Turkish OGID cohort. Thirty-five children with OGID were included in the study. Single gene sequencing, clinical exome analysis, chromosomal microarray analysis and whole exome sequencing were performed. Five pathogenic copy number variants were detected in the patients; three of them located on chromosome 5q35.2 (encompassing NSD1), others on 9q22.3 and 22q13.31. In 19 of 35 patients; we identified pathogenic variants in OGID genes associated with epigenetic regulation, NSD1 (n = 15), HIST1H1E (n = 1), SETD1B (n = 1), and SUZ12 (n = 2). The pathogenic variants in PIK3CA (n = 2), ABCC9 (n = 1), GPC4 (n = 2), FIBP (n = 1), and TMEM94 (n = 1) which had a role in other growth pathways were detected in seven patients. The diagnostic yield was 31/35(88%). Twelve pathogenic variants were novel. The common facial feature of the patients was prominent forehead. The patients with Sotos syndrome were observed to have milder intellectual disability than patients with other OGID syndromes. In conclusion, this study showed, for the first time, that biallelic variants of SUZ12 caused Imagawa-Matsumoto syndrome, monoallelic variants in SETDIB resulted in OGID. Besides expanded the phenotypes of very rare OGID syndromes caused by FIBP and TMEM94

Long-Term Follow-Up Outcomes of 19 Patients with Osteogenesis Imperfecta Type XI and Bruck Syndrome Type I Caused by FKBP10 Variants

Osteogenesis imperfecta type XI (OI-XI) and Bruck syndrome type I (BS1) are two rare disorders caused by biallelic variants in the FKBP10, characterized by early-onset bone fractures and progressive skeletal deformities. The patients with OI-XI, also co-segregated with autosomal-recessive epidermolysis bullosa simplex caused by KRT14 variant, have been reported. In this study, the follow-up clinical features of the patients with OI-XI and BS1 phenotypes due to biallelic FKBP10 variants are compared. The aim of this study is to investigate the follow-up findings of OI-XI and BS1 phenotypes in patients with the FKBP10 variants. A total of 19 children, ten males and nine females, from 16 unrelated families were included in the study. FKBP10 variants were investigated by next-generation sequencing (NGS) based panel gene test or Sanger sequencing. Seventeen patients were followed between 1.5 and 16.8 years, and the last follow-up age was between 2 and 24.6 years (median 10.7 years). They received intravenous bisphosphonate infusions once every 3 months in follow-up period. We identified four different biallelic FKBP10 variants, two of which are novel (c.890_897dup TGATGGAC, p.Gly300Ter and c.1256 + 1G > A) in 16 families. Five of these patients also had findings of epidermolysis bullosa simplex, and the same biallelic c.612T > A (p.Tyr204Ter) variant in KRT14, as well as FKBP10, were identified. Twelve patients were diagnosed with OI-XI; whereas, seven were diagnosed with BS1. The BS1 phenotype was late-onset and the annual fracture number was lower. After bisphosphonate treatment, bone mineral densitometry Z score at L1-L4 increased (p = 0.005) and the number of annual fractures decreased (p = 0.036) in patients with OI-XI. However, no significant effect of bisphosphonate treatment was found on these values in BS1 patients. Despite the treatment, the rate of scoliosis and long bone deformity had increased in both groups at the last examination; and, only two patients could take a few steps with the aid of a walker, while others were not ambulatory, and they used wheelchairs for mobility. We identified two novel variants in FKBP10. Families originating from the same geographic region and having the same variant suggest founder effects. Although the number of fractures decreased with bisphosphonate treatment, none of our patients were able to walk during the follow-up. This study is valuable in terms of showing the follow-up findings of patients with FKBP10 variants for the first time