Response of tomato to fertilizer nutrients integration and herbicides spray: Evaluating growth, yield, fruit quality and herbicides residue

The interaction between fertilizer nutrients and pesticides and their impact on tomato production and quality has been insufficiently studied in tropical agricultural conditions. This research investigated four fertilizer nutrient management (FNM) approaches: major nutrients (NPK), micronutrients, farmyard manure (FYM) and traditional farmer practices (FP), alongside three herbicides—glyphosate, pendimethalin and metribuzin applied using seven methods. Results highlighted the substantial influence of FNM strategies and herbicide applications on tomato growth and yield parameters such as plant height, cluster count, fruits per plant, fruit number and yield per plant. Notably, the NPK+FYM strategy consistently yielded superior results across herbicides and application methods. Individually applied herbicides, particularly glyphosate, exhibited detrimental effects on growth and yield parameters, and the negative impact was conspicuously higher with glyphosate > metribuzin > pendimethalin than with their sequential or combined application. While herbicides decreased tomato yield across FNM practices, the reduction ranged from 1.90–10.95%, 1.79–6.75%, 1.62–6.49% and 1.40–9.10% in NPK, NPK+MN, NPK+FYM and FP treatments, respectively. Fruit quality remained unaffected by FNM practices and herbicides, except for elevated ascorbic acid content and shelf life under NPK+FYM. Herbicide residues in tomato fruits were within permissible limits (below 0.1 mg/kg for glyphosate and 0.05 mg/kg for pendimethalin and metribuzin) across treatments. This study showed that the NPK+FYM practice is the best strategy for increasing the tomato yield and quality parameters besides reducing the herbicide’s toxicity effect on tomato growth at an early stage

The hyperpolarization-activated, cyclic nucleotide-gated channel resides on myocytes in mouse bladders and contributes to adrenergic-induced detrusor relaxation.

Control of urinary continence is predicated on sensory signaling about bladder volume. Bladder sensory nerve activity is dependent on tension, implicating autonomic control over detrusor myocyte activity during bladder filling. Hyperpolarization-activated cyclic nucleotide-gated (HCN) ion channels are known contributors to bladder control, but their mechanism of action is not well understood. The lack of a definitive identification of cell type(s) expressing HCN in the bladder presents a significant knowledge gap. We recently reported a complete transcriptomic atlas of the C57BL/6 mouse bladder showing the dominant HCN paralog in mouse bladder

Loss of resilience contributes to detrusor underactivity in advanced age.

Volume hyposensitivity resulting from impaired sympathetic detrusor relaxation during blad- der filling contributes to detrusor underactivity (DU) associated with aging. Detrusor tension regulation provides an adaptive sensory input of bladder volume to the brainstem and is challenged by physiological stressors superimposed upon biological aging. We recently showed that HCN channels have a stabilizing role in detrusor sympathetic relaxation. While mature mice maintain homeostasis in the face of stressors, old mice are not always capable. In old mice, there is a dichotomous phenotype, in which resilient mice adapt and maintain homeostasis, while non-resilient mice fail to maintain physiologic homeostasis. In this DU model, we used cystometry as a stressor to categorize mice as old-responders (old-R, develop a filling/voiding cycle) or old-non-responders (old-NR, fail to develop a filling/voiding cycle; fluctuating high pressures and continuous leaking), while also assess- ing functional and molecular differences. Lamotrig- ine (HCN activator)-induced bladder relaxation is diminished in old-NR mice following HCN-blockade. Relaxation responses to NS 1619 were reduced in old-NR mice, with the effect lost following HCN- blockade. However, RNA-sequencing revealed no differences in HCN gene expression and electrophysi- ology studies showed similar percentage of detrusor myocytes expressing HCN (Ih) current between old-R and old-NR mice. Our murine model of DU further defines a role for HCN, with failure of adaptive recal- ibration of HCN participation and intensity of HCN- mediated stabilization, while genomic studies show upregulated myofibroblast and fibrosis pathways and downregulated neurotransmitter-degradation path- ways in old-NR mice. Thus, the DU phenotype is multifactorial and represents the accumulation of age- associated loss in homeostatic mechanisms

Histone Acetylome-wide Association Study of Autism Spectrum Disorder.

The association of histone modification changes with autism spectrum disorder (ASD) has not been systematically examined. We conducted a histone acetylome-wide association study (HAWAS) by performing H3K27ac chromatin immunoprecipitation sequencing (ChIP-seq) on 257 postmortem samples from ASD and matched control brains. Despite etiological heterogeneity, ≥68% of syndromic and idiopathic ASD cases shared a common acetylome signature at >5,000 cis-regulatory elements in prefrontal and temporal cortex. Similarly, multiple genes associated with rare genetic mutations in ASD showed common "epimutations." Acetylome aberrations in ASD were not attributable to genetic differentiation at cis-SNPs and highlighted genes involved in synaptic transmission, ion transport, epilepsy, behavioral abnormality, chemokinesis, histone deacetylation, and immunity. By correlating histone acetylation with genotype, we discovered >2,000 histone acetylation quantitative trait loci (haQTLs) in human brain regions, including four candidate causal variants for psychiatric diseases. Due to the relative stability of histone modifications postmortem, we anticipate that the HAWAS approach will be applicable to multiple diseases

Histone Acetylome-wide Association Study of Autism Spectrum Disorder

The association of histone modification changes with autism spectrum disorder (ASD) has not been systematically examined. We conducted a histone acetylome-wide association study (HAWAS) by performing H3K27ac chromatin immunoprecipitation sequencing (ChIP-seq) on 257 postmortem samples from ASD and matched control brains. Despite etiological heterogeneity, ≥68% of syndromic and idiopathic ASD cases shared a common acetylome signature at >5,000 cis-regulatory elements in prefrontal and temporal cortex. Similarly, multiple genes associated with rare genetic mutations in ASD showed common “epimutations.” Acetylome aberrations in ASD were not attributable to genetic differentiation at cis-SNPs and highlighted genes involved in synaptic transmission, ion transport, epilepsy, behavioral abnormality, chemokinesis, histone deacetylation, and immunity. By correlating histone acetylation with genotype, we discovered >2,000 histone acetylation quantitative trait loci (haQTLs) in human brain regions, including four candidate causal variants for psychiatric diseases. Due to the relative stability of histone modifications postmortem, we anticipate that the HAWAS approach will be applicable to multiple diseases.This article is freely available via Open Access. Click on the Additional Link above to access the full-text