Rare earth metallic elements in plants: assessing benefits, risks and mitigating strategies.

Rare earth elements (REEs) comprises of a uniform group of lanthanides and scandium (Sc) and yttrium (Y) finding their key importance in agriculture sectors, electronic and defense industries, and renewable energy production. The immense application of REEs as plant growth promoters has led to their undesirable accumulation in the soil system raising concerns for REE pollution as upcoming stresses. This review mainly addresses the chemistry of REEs, uptake and distribution and their biphasic responses in plant systems and possible plausible techniques that could mitigate/alleviate REE contamination. It extends beyond the present understanding of the biphasic impacts of rare earth elements (REEs) on physio-biochemical attributes. It not only provides landmarks for further exploration of the interrelated phytohormonal and molecular biphasic nature but also introduces novel approaches aimed at mitigating their toxicities. By delving into innovative strategies such as recycling, substitution, and phytohormone-assisted mitigation, the review expands upon existing knowledge of REEs whilst also offering pathways to tackle the challenges associated with REE utilization.

Biomarker-based evaluation of cytogenotoxic potential of glyphosate in Vigna mungo (L.) Hepper genotypes.

Herbicides have proven to be a boon for agricultural fields. Their inherent property to kill weeds and unwanted vegetation makes them an essential biological tool for farmers and agricultural systems. Besides being capable of destroying weeds, they also exhibit certain effects on non-target crop plants. In the present study, a laboratory experiment was performed to assess the effect of glyphosate on Vigna mungo root meristem cells. Seeds of five different genotypes of V. mungo were treated with a series of concentrations of glyphosate ranging from 1 to 10 mM, and their effects on mitotic cell division were studied. Healthy and uniform-sized seeds were selected and were allowed to grow in Petri plates for 3 days, and all the doses were maintained in triplicates. Roots were fixed at day 3 after treatment (DAT) for cytological microscopic slide preparation. The results obtained indicate the dose-dependent reduction in the mitotic index in all the genotypes and an increase in the percentage of chromosomal aberrations (CAs) and relative abnormality rate (RAR). Most commonly observed chromosome aberrations at lower doses (< 6 mM) were fragments, stickiness, and disoriented metaphase, while at higher doses (6 to 10 mM) bridges, laggards, spindle disorientation, and clumping were obvious. The increase in the percentage of CAs and RAR indicates the inhibitory effect of glyphosate on cell cycle progression at various stages in root tip cells. The present study is a fine example of a biomarker-based genotoxic assessment of mitotic damage caused by glyphosate.

Toxicity assessment of metribuzin and its amelioration through plant growth regulators in Vigna radiata (L.) R. Wilczek.

The present experiment was conducted to evaluate the metribuzin-induced stress response in Vigna radiata and to explore the ameliorative role of exogenous application of plant growth regulators (PGRs) against metribuzin toxicity by assessing important biochemical and yield parameters. Prior to the field experiment, dose standardization experiments were performed, and EC50 was calculated for metribuzin. On day 21, field grown V. radiata plants were treated with graded concentrations of metribuzin (0-1000 mg [Formula: see text]). Plants treated with 600 mg [Formula: see text] (EC50) and 1000 mg [Formula: see text] (highest dose) of metribuzin were co-treated individually and simultaneously with gibberellic acid-3 (GA), indole-3 acetic acid (IAA), and salicylic acid (SA). After 7 days of treatment, leaf tissues were analyzed for biochemical parameters, whereas those related to yield were recorded during harvest. The result of this study indicated that metribuzin treatment to V. radiata resulted in increase in lipid peroxidation and reduce chlorophyll and carotenoid contents as well as yield parameters. However, metribuzin-treated plants induced proline accumulation and activity of antioxidant enzymes. Exogenous application of GA, IAA, and SA significantly reduced lipid peroxidation and increased contents of photosynthetic pigments, proline, and antioxidant enzymes thereby increasing yield parameters. It was observed that during metribuzin stress, SA exhibited a better ameliorative response out of the three exogenously applied PGRs, while the combined use of all PGRs exhibited much improved ameliorative response on biochemical and yield parameters of plants.

The RUNX/CBFß Complex in Breast Cancer: A Conundrum of Context.

Dissecting and identifying the major actors and pathways in the genesis, progression and aggressive advancement of breast cancer is challenging, in part because neoplasms arising in this tissue represent distinct diseases and in part because the tumors themselves evolve. This review attempts to illustrate the complexity of this mutational landscape as it pertains to the RUNX genes and their transcription co-factor CBFß. Large-scale genomic studies that characterize genetic alterations across a disease subtype are a useful starting point and as such have identified recurring alterations in CBFB and in the RUNX genes (particularly RUNX1). Intriguingly, the functional output of these mutations is often context dependent with regards to the estrogen receptor (ER) status of the breast cancer. Therefore, such studies need to be integrated with an in-depth understanding of both the normal and corrupted function in mammary cells to begin to tease out how loss or gain of function can alter the cell phenotype and contribute to disease progression. We review how alterations to RUNX/CBFß function contextually ascribe to breast cancer subtypes and discuss how the in vitro analyses and mouse model systems have contributed to our current understanding of these proteins in the pathogenesis of this complex set of diseases.

GRIN2A mutations cause epilepsy-aphasia spectrum disorders.

Epilepsy-aphasia syndromes (EAS) are a group of rare, severe epileptic encephalopathies of unknown etiology with a characteristic electroencephalogram (EEG) pattern and developmental regression particularly affecting language. Rare pathogenic deletions that include GRIN2A have been implicated in neurodevelopmental disorders. We sought to delineate the pathogenic role of GRIN2A in 519 probands with epileptic encephalopathies with diverse epilepsy syndromes. We identified four probands with GRIN2A variants that segregated with the disorder in their families. Notably, all four families presented with EAS, accounting for 9% of epilepsy-aphasia cases. We did not detect pathogenic variants in GRIN2A in other epileptic encephalopathies (n = 475) nor in probands with benign childhood epilepsy with centrotemporal spikes (n = 81). We report the first monogenic cause, to our knowledge, for EAS. GRIN2A mutations are restricted to this group of cases, which has important ramifications for diagnostic testing and treatment and provides new insights into the pathogenesis of this debilitating group of conditions.

Targeted resequencing in epileptic encephalopathies identifies de novo mutations in CHD2 and SYNGAP1.

Epileptic encephalopathies are a devastating group of epilepsies with poor prognosis, of which the majority are of unknown etiology. We perform targeted massively parallel resequencing of 19 known and 46 candidate genes for epileptic encephalopathy in 500 affected individuals (cases) to identify new genes involved and to investigate the phenotypic spectrum associated with mutations in known genes. Overall, we identified pathogenic mutations in 10% of our cohort. Six of the 46 candidate genes had 1 or more pathogenic variants, collectively accounting for 3% of our cohort. We show that de novo CHD2 and SYNGAP1 mutations are new causes of epileptic encephalopathies, accounting for 1.2% and 1% of cases, respectively. We also expand the phenotypic spectra explained by SCN1A, SCN2A and SCN8A mutations. To our knowledge, this is the largest cohort of cases with epileptic encephalopathies to undergo targeted resequencing. Implementation of this rapid and efficient method will change diagnosis and understanding of the molecular etiologies of these disorders.