We have developed and tested a new method for nondestructive estimation of chlorophyll- and nitrogen-contents in rye leaf. It was found that the relationships among nitrogen, chlorophyll content and fresh weight were significantly positive correlated. Nitrogen and chlorophyll content were positively correlated whereas correlation coefficients among R, G, R-B and G-B on the basis of photo-numerical values were negative. We have found that R/(R-B) obtained from data of digital camera is the best criterion to estimate the chlorophyll content of leaves. The regression curves of the relation between R/(R-B) and chlorophyll content were also calculated from the data collected on cloudy days. The coefficients of determination (r²) were ranged from 0.33 to 0.99. In this study, the accuracy in estimating chlorophyll content from the color data of digital camera image could be improved by correcting with R, G, and B values. It is suggested that, for practical purposes, the image values estimated with sufficient accuracy using a portable digital camera can be applied for determining chlorophyll content and nitrogen status in plant leaves.
Stargardt disease type 1 (STGD1) is the most common hereditary form of maculopathy and remains untreatable. STGD1 is caused by biallelic variants in the ABCA4 gene, which encodes the ATP-binding cassette (type 4) protein (ABCA4) that clears toxic byproducts of the visual cycle. The c.5461-10T>C p.[Thr1821Aspfs∗6,Thr1821Valfs∗13] variant is the most common severe disease-associated variant, and leads to exon skipping and out-of-frame ABCA4 transcripts that prevent translation of functional ABCA4 protein. Homozygous individuals typically display early onset STGD1 and are legally blind by early adulthood. Here, we applied antisense oligonucleotides (AONs) to promote exon inclusion and restore wild-type RNA splicing of ABCA4 c.5461-10T>C. The effect of AONs was first investigated in vitro using an ABCA4 midigene model. Subsequently, the best performing AONs were administered to homozygous c.5461-10T>C 3D human retinal organoids. Isoform-specific digital polymerase chain reaction revealed a significant increase in correctly spliced transcripts after treatment with the lead AON, QR-1011, up to 53% correct transcripts at a 3 μM dose. Furthermore, western blot and immunohistochemistry analyses identified restoration of ABCA4 protein after treatment. Collectively, we identified QR-1011 as a potent splice-correcting AON and a possible therapeutic intervention for patients harboring the severe ABCA4 c.5461-10T>C variant. Stargardt disease type 1 (STGD1) is the most common hereditary form of maculopathy and remains untreatable. STGD1 is caused by biallelic variants in the ABCA4 gene, which encodes the ATP-binding cassette (type 4) protein (ABCA4) that clears toxic byproducts of the visual cycle. The c.5461-10T>C p.[Thr1821Aspfs∗6,Thr1821Valfs∗13] variant is the most common severe disease-associated variant, and leads to exon skipping and out-of-frame ABCA4 transcripts that prevent translation of functional ABCA4 protein. Homozygous individuals typically display early onset STGD1 and are legally blind by early adulthood. Here, we applied antisense oligonucleotides (AONs) to promote exon inclusion and restore wild-type RNA splicing of ABCA4 c.5461-10T>C. The effect of AONs was first investigated in vitro using an ABCA4 midigene model. Subsequently, the best performing AONs were administered to homozygous c.5461-10T>C 3D human retinal organoids. Isoform-specific digital polymerase chain reaction revealed a significant increase in correctly spliced transcripts after treatment with the lead AON, QR-1011, up to 53% correct transcripts at a 3 μM dose. Furthermore, western blot and immunohistochemistry analyses identified restoration of ABCA4 protein after treatment. Collectively, we identified QR-1011 as a potent splice-correcting AON and a possible therapeutic intervention for patients harboring the severe ABCA4 c.5461-10T>C variant.
The levels of polyamines were measured to investigate the alternative nitrogen metabolism during maturation and sprouting in rice. The rice plants (cv. Ansanbyeo) were cultivated in 20-year-old non-fertilized field. The flag leaves and spikes were collected weekly after the earing stage and the seeds were harvested daily after lodging. Free, bound, and conjugated polyamines were analyzed using reverse phase HPLC. Putrescine, spermidine, spermine, agmatine and tyramine were the major amines found in rice. The level of stress-induced amine, putrescine increased during the preharvest sprouting confirming that the process was a stress to the plants. With all other polyamines, tyramine in free form decreased in flag leaves and panicles during seed maturation. However, agmatine in bound form showed a noticeable increase about 8-fold during 6 weeks period of maturation after which it declined to the bottom level. Among the individual amines, tyramine and spermine in conjugated form showed a marked change during matutation and sprouting. Interestingly, the level of tyramine with all conjugated polyamine decreased in spikes during seed maturation and increased during preharvest sprouting implying that tyrosine decarboxyation and conjugation to phenolic acids may play a key role in preharvest sprouting. Spermine in conjugated form was synthesized only at the early earing stage in the level of fresh weight, and then decreased to the level of nmole during maturation. Thereafter, it dramatically increased to 2.8 mole during preharvest sprouting. In this study we found the tyramine is a major amine in rice, and it would play a critical role in N-assimilation during seed maturation and sprouting.
Recent studies have strongly implicated postsynaptic scaffolding proteins such as SAPAP3 or Shank3 in the pathogenesis of various mood disorders, including autism spectrum disorder, bipolar disorder (BD), and obsessive-compulsive disorders. Neural Abelson-related gene-binding protein 2 (nArgBP2) was originally identified as a protein that interacts with SAPAP3 and Shank3. Recent study shows that the genetic deletion of nArgBP2 in mice leads to manic/bipolar-like behavior resembling symptoms of BD. However, the function of nArgBP2 at synapse, or its connection with the synaptic dysfunctions, is completely unknown. This study provides compelling evidence that nArgBP2 regulates the spine morphogenesis through the activation of Rac1/WAVE/PAK/cofilin pathway, and that its ablation causes a robust and selective inhibition of excitatory synapse formation, by controlling actin dynamics. Our results revealed the underlying mechanism for the synaptic dysfunction caused by nArgBP2 downregulation that associates with analogous human BD. Moreover, since nArgBP2 interacts with key proteins involved in various neuropsychiatric disorders, our finding implies that nArgBP2 could function as a hub linking various etiological factors of different mood disorders.
Despite the complex genetic architecture, a broad spectrum of psychiatric disorders can still be caused by mutation(s) in the same gene. These disorders are interrelated with overlapping causative mechanisms including variations in the interaction among the risk-associated proteins that may give rise to the specific spectrum of each disorder. Additionally, multiple lines of evidence implicate an imbalance between excitatory and inhibitory neuronal activity (E/I imbalance) as the shared key etiology. Thus, understanding the molecular mechanisms underlying E/I imbalance provides essential insight into the etiology of these disorders. One important class of candidate risk genes is the postsynaptic scaffolding proteins, such as nArgBP2, SAPAP, and SHANK that regulate the actin cytoskeleton in dendritic spines of excitatory synapses. This review will cover and discuss recent studies that examined how these proteins, especially nArgBP2, are associated with psychiatric disorders. Next, we propose a possibility that variations in the interaction among these proteins in a specific brain region might contribute to the onset of diverse phenotypes of psychiatric disorders. The assembly of scaffolding proteins, key regulators of many signaling pathways, found in the brain’s synapses underpin a diverse range of neuropsychiatric disorders. Sunghoe Chang and colleagues from Seoul National University, South Korea, review how these postsynaptic proteins regulate the cellular cytoskeleton in nerve cell protrusions to maintain the balance between excitatory and inhibitory inputs in the brain. They discuss how perturbations in three particular proteins can cause an imbalance in synaptic signals that leads to conditions such as bipolar disorder, schizophrenia and autism. The authors propose that these proteins form a “core scaffolding triad” and interact in different ways to cause different mental illnesses. Dysregulation of these proteins could explain how mutations in the same genes, depending on whether they boost or decrease gene expression, contribute to the onset of diverse psychiatric disorders.
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