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Cotton (Gossypium spp.) is a vital global source of renewable fiber and ranks among the world's most important cash crops. While extensive nuclear genomic data of Gossypium has been explored, the organellar genomic resources of allotetraploid cotton, remain largely untapped at the population level. The plastid genome (plastome) is well suited for studying plant species relationships and diversity due to its nonrecombinant uniparental inheritance. Here, we conducted de novo assembly of 336 Gossypium plastomes, mainly from domesticated cultivars, and generated a pan‐plastome level resource for population structure and genetic diversity analyses. The assembled plastomes exhibited a typical quadripartite structure and varied in length from 160 103 to 160 597 bp. At the species level, seven allotetraploid species were resolved into three clades, where Gossypium tomentosum and Gossypium mustelinum formed an early diverging clade rooted by diploids, followed by splitting two sister clades of Gossypium darwinii–Gossypium barbadense and Gossypium hirsutum–Gossypium ekmanianum–Gossypium stephensii. Within the G. hirsutum clade the resolution of cultivated accessions was less polyphyletic with landrace and wild accessions than in G. barbadense suggesting some selection on plastome in the domestication of this adaptable species of cotton. The nucleotide diversity of G. hirsutum was higher than that of G. barbadense. We specifically compared the plastomes of G. hirsutum and G. barbadense to find mutational hotspots within each species as potential molecular markers. These findings contribute a valuable resource for exploring cotton evolution as well as in the breeding of new cotton cultivars and the preservation of wild and cultivated germplasm. [ABSTRACT FROM AUTHOR]

In this work, one-dimensional Ni-rich LiNi0.6Co0.2Mn0.2O2 microrod cathode material for lithium-ion battery has been firstly prepared by a simple stepwise oxalate co-precipitation method. Rod-like CoC2O4·2H2O formed in the first process is served as template for the formation of MC2O4·2H2O (M=Ni, Co, Mn) precursor, and the morphology of rod-like is maintained after the heat treatment with Li2CO3. The crystalline structure and morphology of the samples are characterized by XRD, SEM, and TEM/HRTEM. The electrochemical performances are evaluated by galvanostatic charge/discharge tests. With the beneficiation of micro/nanostructure, the LiNi0.6Co0.2Mn0.2O2 microrod cathode material shows an initial discharge capacity of 162, 134, 117, and 105 mAh g−1 at 0.1 °C, 1 °C, 3 °C, and 5 °C, respectively, and maintains 72.8% of its initial discharge capacity after 100 cycles at 1 °C. [ABSTRACT FROM AUTHOR]

Our previous study has shown heme oxygenase-1 (HO-1) protects human lens epithelial cells (LECs) against H 2 O 2 -induced oxidative stress and apoptosis. Nrf2, the major regulator of HO-1, is triggered during the mutual induction of oxidative stress and ER stress. In response to ER stress, unfolded protein response (UPR) serves as a program of transcriptional and translational regulation mechanism with PERK involved. Both Nrf2 and ATF4 are activated as the downstream effect of PERK signaling coordinating the convergence of dual stresses. However, the ways in which Nrf2 interacting with ATF4 regulates deteriorated redox state have not yet been fully explored. Here, the transfected LECs with Nrf2 overexpression illustrated enhanced resistance in morphology and viability upon H 2 O 2 treatment condition. Intracellular ROS accumulation arouses ER stress, initiating PERK dependent UPR and inducing the downstream signal Nrf2 and ATF4 auto-phosphorylation. Further, converging at target promoters, ATF4 facilitates Nrf2 with the expression of ARE-dependent phase II antioxidant and detoxification enzymes. According to either Nrf2 or ATF4 gene modification, our data suggests a novel interaction between Nrf2 and ATF4 under oxidative and ER stress, thus drives specific enzymatic and non-enzymatic reactions of antioxidant mechanisms maintaining redox homeostasis. Therapies that restoring Nrf2 or ATF4 expression might help to postpone LECs aging and age-related cataract formation. [ABSTRACT FROM AUTHOR]