Notes

Multi-objective signifiant novo molecular design of natural and organic structure-directing providers with regard to zeolites employing nature-inspired ould like nest optimization.
Here we report the 409.5 Mb chromosome-level assembly of the first bred semi-dwarf rice, the Taichung Native 1 (TN1), which served as the template for the development of the Green Revolution (GR) cultivar IR8 "miracle rice". We sequenced the TN1 genome utilizing multiple platforms and produced PacBio long reads, Illumina paired-end reads, Illumina mate-pair reads and 10x Genomics linked reads. We used a hybrid approach to assemble the 226× coverage of sequences by a combination of de novo and reference-guided approaches. The assembled TN1 genome has an N50 scaffold size of 33.1 Mb with the longest measuring 45.5 Mb. We annotated 37,526 genes, in which 24,102 (64.23%) were assigned Blast2GO annotations. The genome has 4672 or 95.4% complete BUSCOs and a repeat content of 51.52%. We developed our own method of creating a GR pangenome using the orthologous relationships of the proteins of TN1, IR8, MH63 and IR64, identifying 16,999 core orthologue groups of Green Revolution. From the pangenome, we identified a set of shared and unique gene ontology terms for the accessory clusters, characterizing TN1, IR8, MH63 and IR64. This TN1 genome assembly and GR pangenome will be a resource for new genomic discoveries about Green Revolution, and for improving the disease and insect resistances and the yield of rice.Colletotrichum, a hemibiotrophic fungal pathogen with a broad host range, causes a yield-limiting disease called anthracnose. Stylo (Stylosanthes) is a dominant pasture legume in tropics and subtropics, and anthracnose is one of its most destructive disease. Resistance mechanisms against anthracnose in stylo are poorly understood, thus hindering the development of resistant varieties. We performed time-resolved leaf transcriptomics, metabolomics and in vitro inhibition assay to investigate the defense responses against Colletotrichum gloeosporioides in stylo. Transcriptomics demonstrated that flavonoid biosynthetic genes were significantly induced during the infection. Consistently, metabolomics also showed the increased accumulation of flavonoid compounds. In vitro assays showed that phloretin and naringenin inhibited the mycelial growth, and apigenin, daidzein, quercetin and kaempferol suppressed conidial germination of Colletotrichum strains. Together, our results suggest that stylo plants cope with C. gloeosporioides by up-regulation of genes and compounds in flavonoid biosynthesis pathway, providing potential targets for resistance breeding.Pterocarya stenoptera is a tree species that occurs along rivers and has high tolerance to waterlogging. Identification of waterlogging response genes in the aboveground part of P. stenoptera will increase understanding of tolerance mechanisms under root waterlogging conditions. In this study, we employed four physiological indicators and comparative transcriptome sequencing to investigate the waterlogging tolerance mechanism in P. Bortezomib datasheet stenoptera. The physiological results showed that the aboveground part of P. stenoptera was not obviously affected by waterlogging. P. stenoptera enhanced waterlogging tolerance by increasing the synthesis of alpha-Linolenic acids and flavonoids and activating the jasmonic acid, ethylene, and auxin signaling pathways. Our results confirmed our hypothesis that P. stenoptera, a species that is widely distributed along rivers, has evolved a range of mechanisms in response to waterlogging. Our research will provide new insights for understanding the tolerance mechanism of species to waterlogging.Epigenetic gene silencing of the tumor suppressor death-associated protein kinase 1 (DAPK1) is implicated in the progression of malignant gliomas. However, the mechanism underlying the repression of DAPK1 in gliomas remains elusive. In this study, we identified the existence of DAPK1-inositol 1,4,5-trisphosphate receptor (IP3R)-interacting protein (ITPRIP) -myosin regulatory light polypeptide 9 (MYL9) complex in malignant glioma cells. Lentivirus co-infection and coimmunoprecipitation showed that ITPRIP bound with the death domain (DD) of DAPK1 in vitro. Further, dissociating ITPRIP-DAPK1 interaction inhibited glioma tumor growth in vitro but not in vivo. Moreover, knockdown of ITPRIP or DAPK1 impaired the ternary complex formation, whereas MYL9 knockdown did not affect ITPRIP-DAPK1 association. We further found that ITPRIP recruited MYL9 to the kinase domain (KD) of DAPK1, and in turn impeded the phosphorylation of MYL9. Accordingly, interference of ITPRIP enhanced the suppressive effects of DAPK1-KD on glioma progression both in vitro and in vivo. Our results demonstrate that ITPRIP plays a crucial role in the inhibition of DAPK1 and enhancement of tumorigenic properties of malignant glioma cells.Migraine is a common but poorly understood sensory circuit disorder. Mouse models of familial hemiplegic migraine (FHM, a rare monogenic form of migraine with aura) show increased susceptibility to cortical spreading depression (CSD, the phenomenon that underlies migraine aura and can activate migraine headache mechanisms), allowing an opportunity to investigate the mechanisms of CSD and migraine onset. In FHM type 2 (FHM2) knock-in mice with reduced expression of astrocytic Na+, K+-ATPases, the reduced rate of glutamate uptake into astrocytes can account for the facilitation of CSD initiation. Here, we investigated the underlying mechanisms and show that the reduced rate of glutamate clearance in FHM2 mice results in increased amplitude and slowing of rise time and decay of the NMDA receptor (NMDAR) excitatory postsynaptic current (EPSC) elicited in layer 2/3 pyramidal cells by stimulation of neuronal afferents in somatosensory cortex slices. The relative increase in NMDAR activation in FHM2 mice is activity-dependent, being larger after high-frequency compared to low-frequency afferent activity. Inhibition of GluN1-N2B NMDARs, which hardly affected the NMDAR EPSC in wild-type mice, rescued the increased and prolonged activation of NMDARs as well as the facilitation of CSD induction and propagation in FHM2 mice. Our data suggest that the enhanced susceptibility to CSD in FHM2 is mainly due to specific activation of extrasynaptic GluN1-N2B NMDARs and point to these receptors as possible therapeutic targets for prevention of CSD and migraine.
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