Single-cell transcriptome atlas reveals spatiotemporal developmental trajectories in the basal roots of moso bamboo (Phyllostachys edulis)

Roots are essential for plant growth and development.Bamboo is a large Poaceae perennial with 1642 species worldwide.However,little is known about the transcriptional atlas that underpins root cell-type differentiation.Here,we set up a modified protocol for protoplast preparation and report single-cell transcriptomes of 14279 filtered single cells derived from the basal root tips of moso bamboo.We identified four cell types and defined new cell-type-specific marker genes for the basal root.We reconstructed the developmental trajectories of the root cap,epidermis,and ground tissues and elucidated critical factors regulating cell fate determination.According to in situ hybridization and pseudotime trajectory analysis,the root cap and epidermis originated from a common initial cell lineage,revealing the particularity of bamboo basal root development.We further identified key regulatory factors for the differentiation of these cells and indicated divergent root developmental pathways between moso bamboo and rice.Additionally,PheWOX13a and PheWOX13b ectopically expressed in Arabidopsis inhibited primary root and lateral root growth and regulated the growth and development of the root cap,which was different from WOX13 orthologs in Arabidopsis.Taken together,our results offer an important resource for investigating the mechanism of root cell differentiation and root system architecture in perennial woody species of Bambusoideae.

Exchange-coupling-induced fourfold magnetic anisotropy in CoFeB/FeRh bilayer grown on SrTiO_(3)(001)

Exchange coupling across the interface between a ferromagnetic(FM)layer and an antiferromagnetic(AFM)or another FM layer may induce a unidirectional magnetic anisotropy and/or a uniaxial magnetic anisotropy,which has been extensively studied due to the important application in magnetic materials and devices.In this work,we observed a fourfold magnetic anisotropy in amorphous Co Fe B layer when exchange coupling to an adjacent Fe Rh layer which is epitaxially grown on an SrTiO_(3)(001)substrate.As the temperature rises from 300 K to 400 K,Fe Rh film undergoes a phase transition from AFM to FM phase,the induced fourfold magnetic anisotropy in the Co Fe B layer switches the orientation from the Fe Rh<110>to Fe Rh<100>directions and the strength is obviously reduced.In addition,the effective magnetic damping as well as the two-magnon scattering of the Co Fe B/Fe Rh bilayer also remarkably increase with the occurrence of magnetic phase transition of Fe Rh.No exchange bias is observed in the bilayer even when Fe Rh is in the nominal AFM state,which is probably because the residual FM Fe Rh moments located at the interface can well separate the exchange coupling between the below pinned Fe Rh moments and the Co Fe B moments.

KLF4 facilitates chromatin accessibility remodeling in porcine early embryos

Chromatin accessibility remodeling driven by pioneer factors is critical for the development of early embryos.Current studies have illustrated several pioneer factors as being important for agricultural animals,but what are the pioneer factors and how the pioneer factors remodel the chromatin accessibility in porcine early embryos is not clear.By employing low-input DNase-seq(liDNase-seq),we profiled the landscapes of chromatin accessibility in porcine early embryos and uncovered a unique chromatin accessibility reprogramming pattern during porcine preimplantation development.Our data revealed that KLF4 played critical roles in remodeling chromatin accessibility in porcine early embryos.Knocking down of KLF4 led to the reduction of chromatin accessibility in early embryos,whereas KLF4 overexpression promoted the chromatin openness in porcine blastocysts.Furthermore,KLF4 deficiency resulted in mitochondrial dysfunction and developmental failure of porcine embryos.In addition,we found that overexpression of KLF4 in blastocysts promoted lipid droplet accumulation,whereas knockdown of KLF4 disrupted this process.Taken together,our study revealed the chromatin accessibility dynamics and identified KLF4 as a key regulator in chromatin accessibility and cellular metabolism during porcine preimplantation embryo development.

Water-soluble Cu30 nanoclusters as a click chemistry catalyst for living cell labeling via azide-alkyne cycloaddition

Cu(I)-catalyzed azide-alkyne cycloadditions(CuAAC)have gained increasing interest in the selective labeling of living cells and organisms with biomolecules.However,their application is constrained either by the high cytotoxicity of Cu(I)ions or the low activity of CuAAC in the internal space of living cells.This paper reports the design of a novel Cu-based nanocatalyst,watersoluble thiolated Cu30 nanoclusters(NCs),for living cell labeling via CuAAC.The Cu30 NCs offer good biocompatibility,excellent stability,and scalable synthesis(e.g.,gram scale),which would facilitate potential commercial applications.By combining the highly localized Cu(I)active species on the NC surface and good structural stability,the Cu30 NCs exhibit superior catalytic activities for a series of Huisgen cycloaddition reactions with good recyclability.More importantly,the biocompatibility of the Cu30 NCs enables them to be a good catalyst for CuAAC,whereby the challenging labeling of living cells can be achieved via CuAAC on the cell membrane.This study sheds light on the facile synthesis of atomically precise Cu NCs,as well as the design of novel Cu NCs-based nanocatalysts for CuAAC in intracellular bioorthogonal applications.

H3K27me3 shapes DNA methylome by inhibiting UHRF1-mediated H3 ubiquitination

DNA methylation and histone lysine tri-methylation at H3K27(H3K27me3)are two chromatin modifications for transcriptional gene silencing,which play important roles in diverse biological processes,including cell fate determination and cell lineage commitment.These two marks are largely mutually exclusive and target distinct sets of genes in the mammalian genome.However,how H3K27me3 shapes the DNA methylome remains elusive.Here,we report that the loss of H3K27me3 modification leads to increased DNA methylation at previously marked H3K27me3 sites,indicating that H3K27me3 negatively regulates DNA methylation.Genome-wide analysis of H3 ubiquitination,essential for recruitment and activation of DNA methyltransferase DNMT1,reveals the absence of H3 ubiquitination at H3K27me3 marked nucleosomes.Moreover,loss of H3K27me3 modification induces an increase in H3K18 ubiquitination at the corresponding hyper-methylated loci.Importantly,we show that H3K27me3 directly inhibits UHRF1-mediated H3 ubiquitination toward nucleosomes in a defined biochemical assay.Taken together,our findings reveal a general mechanism for H3K27me3-mediated shaping of the mammalian DNA methylome via modulation of H3 ubiquitination.