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Cues of maternal and paternal origins interact to control seed development, and the underlying molecular mechanisms are still far from clear. Here, we show that TOPOISOMERASE Iα (TOP1α), UP-FRAMESHIFT SUPPRESSOR 1 (UPF1), and TRANSPARENT TESTA GLABRA2 (TTG2) gametophytically, biparentally regulate seed size in Arabidopsis. TOP1α and UPF1 are mainly expressed in antipodal cells, and loss of their function leads to ectopic TTG2 expression in these female gametophytic cells. We further demonstrate that TOP1α and UPF1 directly repress TTG2 expression through affecting its chromatin status and determine its relative expression in antipodal cells versus sperm cells, which controls seed size in a dosage-dependent and parent-of-origin-dependent manner. The molecular interplay among these three genes explains their biparental gametophytic effect during diploidy and interploidy reciprocal crosses. Taken together, our findings reveal a molecular framework of parental interaction for seed size control. Cues of maternal and paternal origin interact to control seed development, and the underlying molecular mechanisms are still far from clear. This study shows that in Arabidopsis, the relative dosage of the transcription factor TTG2 between antipodal cells and sperm cells at the beginning of seed development determines seed size under the control of TOP1α and UPF1. [ABSTRACT FROM AUTHOR]

Background: Hepatocellular carcinoma (HCC) is an aggressive primary hepatic cancer with high malignancy and poor prognosis. Long noncoding RNA HOTAIR has been classified as an oncogene to accelerate cell proliferation, migration, and invasion in many cancer types by interacting with the miRNA. Therefore, we assumed that HOTAIR might participate in HCC cell progression by interacting with miR-217-5p expression. Materials and Methods: The expression of HOTAIR and miR-217-5p in 35 HCC patients and HCC cells was measured by quantitative real-time polymerase chain reaction. Cell transfection was conducted using Lipofectamine 2000 transfection reagent. CCK8 and flow cytometry was applied for the measurement of cell proliferation and apoptosis. Cell migration and invasion capacities were carried out by transwell assay. Xenograft mice were constructed by subcutaneously injecting of stably transfected Huh-7 cells in mice. The interaction between HOTAIR and miR-217-5p was determined by luciferase reporter system. Protein expression of P13K, p-P13K, AKT, p-AKT, MMP-2, and MMP-9 was analyzed using Western blot assay. Results: The expression of HOTAIR was upregulated, whereas miR-217-5p was downregulated in HCC tumor tissues and cell lines (Hep3B and Huh-7) compared with normal tissues and human normal liver cell line MIHA. In addition, HOTAIR expression was negatively correlated with miR-217-5p expression in HCC (r2 = 0.1867, p = 0.0171). More importantly, HOTAIR knockdown induced apoptosis and inhibited cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT). In vivo experiments revealed that the interference of HOTAIR inhibited tumor growth. Subsequently, luciferase reporter system confirmed the interaction between HOTAIR and miR-217-5p. The rescue experiments clarified that miR-217-5p inhibitor attenuated the suppression of HOTAIR silencing on HCC cell proliferation, migration, invasion, and EMT. Furthermore, miR-217-5p inhibitor restored the inhibition of HOTAIR silencing mediated p-PI3K/p-AKT/MMP-2/9 protein expression. Conclusions:HOTAIR contributes to cell progression in HCC by sponging miR-217-5p, representing promising biomarkers for HCC treatment. [ABSTRACT FROM AUTHOR]

To address the risk of spoofing the information exchanged by users and reduce the trustworthiness of third party, we propose a quantum information fair exchange protocol based on three-particle GHZ states. This protocol achieves quantum multi-party fair exchange of secret information through the utilization of three-particle GHZ states, Pauli matrix, a semi-trusted third party, and polarization state of a single photon. By leveraging the unique physical properties of the GHZ state, this protocol achieves fair exchange of secret information with experimental results that align with theoretical derivation, thus demonstrating its feasibility. Additionally, it provides superdense coding which enhances transmission efficiency while also being resistant to false signal attacks, interception retransmission attacks, and entanglement attacks, ultimately improving security. Furthermore, compared with the classic fair exchange protocol, which requires a trusted third party, it only requires a semi-trusted third party, which raises the security from "computational security" to "unconditional security". The implementation of this protocol resolves the risk of users who hand over information first, presenting a novel solution for digital currency trading, information swapping, and multi-party secure computing. [ABSTRACT FROM AUTHOR]

Most genes identified that control Arabidopsis trichome initiation and formation are transcription factors or regulatory components in transcriptional networks and include GLABROUS1 (GL1), GLABRA2 (GL2), GLABRA3 (GL3) and TRANSPARENT TESTA GLABRA1 (TTG1). Herein, we report that an importin β-like protein, SENSITIVE TO ABA AND DROUGHT2 (SAD2), is required for trichome initiation. Mutations in SAD2 disrupted trichome initiation resulting in reduced trichome number, but had no effect on trichome development or root hair number and development. Expression levels of GL1, MYB23, GL2 and TTG1 were reduced in shoots of sad2 mutants while expression levels of GL3 and ENHANCER OF GLABRA3 ( EGL3) were enhanced. Overexpression of GL3 increased trichome numbers in wild type but not in sad2 mutants, indicating that the function of the GL3 protein is altered in the sad2 mutants. In contrast, overexpression of GFP-GL1 decreased trichome number in both wild type and sad2. Double mutant analysis of gl1 sad2 and gl3 sad2 indicated that SAD2 functions genetically, at least in part, in the same pathway with these two genes. Co-immunoprecipitation indicated that the sad2 mutation does not disrupt formation of the TTG1-GL3-GL1 complex. Analysis of GFP fusions of GL1, GL2, GL3 and TTG1 suggested that these proteins are most likely not direct cargo of SAD2. Our data suggest that SAD2 is involved in trichome initiation by regulating these nuclear genes. [ABSTRACT FROM AUTHOR]

Abstract: DNA damage stabilizes and activates p53, which selectively induces downstream targets to modulate the cellular response. As a homeostatic regulator of cell cycle checkpoint, the p53 target Wip1 plays essential roles in releasing cells from DNA damage-induced checkpoints after appropriate repair of the damaged-DNA. It is unknown how Wip1 performs when the DNA damage is beyond repair. Here we address that Wip1 displays dose-dependent responses to UVC irradiation. A low dose of UVC, which stimulates intra-S phase cell cycle arrest, transiently induces the Wip1 protein levels in a p53-dependent manner. In contrast, a high dose of UVC, which induces apoptosis, suppresses the Wip1 protein levels in a p53-independent manner. The UVC dose-dependent response of Wip1 correlates not only with the cellular response but also with the activity of p53. Wip1 dephosphorylates p53 on its Ser15 residue. However, the mutual regulation between Wip1 and p53 is only triggered by a low dose of UVC. In response to a high dose of UVC, the sustained activation of p53 fails to induce the downstream targets, including Wip1, Mdm2, p21 and GADD45α. Nonetheless, the reduced Wip1 level contributes to the sustained accumulation of phospho-p53 (Ser15) in response to a high dose of UVC. Our results suggest that Wip1 is regulated by UVC in a dose-dependent manner. Moreover, the mutual regulation between Wip1 and p53 is highly dose-dependent upon UVC irradiation, and this contributes to the different outcomes of the cellular response to UVC. [Copyright &y& Elsevier]

Plants exhibit different flowering behaviors in response to variable photoperiods across a wide geographical range. Here, we identify MYC3, a bHLH transcription factor, and its cis -element form the long-sought regulatory module responsible for cis -regulatory changes at the florigen gene FLOWERING LOCUS T (FT) that mediate natural variation in photoperiodic flowering responses in Arabidopsis. MYC3 is stabilized by DELLAs in the gibberellin pathway to suppress FT through binding the ACGGAT motif and antagonizing CONSTANS (CO) activation. Changing photoperiods modulate the relative abundance of MYC3 and CO, thus determining either of them as the predominant regulator for FT expression under different day lengths. Cis -regulatory changes in the MYC3 binding site at FT are associated with natural variation in day-length requirement for flowering in Arabidopsis accessions. Our findings reveal that environmental and developmental signals converge at MYC3 suppression of FT , an elementary event underlying natural variation in photoperiodic flowering responses. • MYC3 represses flowering through antagonizing CO to regulate FT expression • MYC3 is stabilized by DELLAs in the gibberellin pathway • Changing photoperiods modulate the relative abundance of MYC3 and CO • Natural variation of the MYC3 binding site at FT affects photoperiodic flowering Plants exhibit different flowering behaviors under variable day lengths. Bao et al. demonstrate that day length and the phytohormone gibberellin control flowering time through the regulatory protein MYC3 in Arabidopsis. Changes in the MYC3 binding site at the florigen gene FT contribute to natural variation in day-length requirement for flowering. [ABSTRACT FROM AUTHOR]