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Light is a critical external signal for seed germination. The photoreceptor phytochrome B (PHYB) perceives light stimulation and promotes seed germination during the early phase after imbibition. SOM is a CCH-type zinc finger protein and negatively regulates PHYB-mediated seed germination by controlling downstream gibberellic acid (GA) and abscisic acid (ABA) metabolism. As a small molecular signal, carbon monoxide (CO) has been reported to regulate seed germination under environmental stress, but the underlying mechanism remains unclear. In this study, we first found that CO enhanced PHYB-dependent seed germination, and red light irradiation increased the transcriptional level of gene encoding Heme oxygenase 1(HY1) for CO production, this process required PHYB. Pharmacological and genetic analyses revealed that CO signals repressed the transcriptional level of SOM to alter downstream GA/ABA metabolism related genes expression, ultimately relieving the inhibitory effect of SOM on seed germination. Furthermore, CO signals possibly recruited histone deacetylase 6 (HDA6) to the promoter region of SOM to decrease its expression by diminishing histone H3 acetylation levels at this locus. Taken together, our results propose a novel mechanism for CO signals in promoting light-initiated seed germination via recruiting HDA6 to epigenetically regulate SOM expression., (Copyright © 2018 Elsevier B.V. All rights reserved.)

Purpose: Angiogenesis is involved in many pathological and physiological processes and is mainly driven by hypoxia. Karyopherin subunit alpha 2 (KPNA2), a member of the nuclear transport protein family, was recently shown to be induced by hypoxia in various types of tumours, so we aimed to investigate the role and mechanism of KPNA2 in angiogenesis under hypoxia. Materials and methods: After overexpression or knockdown of KPNA2 in human umbilical vein endothelial cells (HUVEC) by adenovirus vector infection, the tube formation, proliferation and migration of HUVEC under hypoxia were detected by tubule formation assay, 5-ethynyl-2′-deoxyuridine (EdU) staining and Transwell assay, respectively. After overexpression or knockdown of KPNA2 in a murine hindlimb ischemia model by local injection of purified adenovirus vector into the gastrocnemius muscle, blood flow changes were examined with a laser Doppler system. Changes in KPNA2-binding proteins under hypoxia were detected by immunoprecipitation-mass spectrometry (IP-MS) and co-immunoprecipitation (Co-IP). The effect of KPNA2 on signal transducer and activator of transcription 3 (STAT3) was detected by Western blotting and quantitative RT‒PCR. Results: KPNA2 was upregulated in the HUVEC hypoxia model and murine hindlimb ischemia model. Overexpression of KPNA2 increased the proliferation, migration and tube formation of HUVEC under hypoxia, while knockdown of KPNA2 reduced the proliferation, migration and tube formation of HUVEC. Overexpression of KPNA2 promoted the restoration of blood flow in the murine hindlimb ischemia model, while knockout of KPNA2 inhibited the restoration of blood flow in the murine hindlimb ischemia model. Mechanistically, hypoxia promoted the binding of STAT3 to KPNA2. Overexpression of KPNA2 promoted STAT3 phosphorylation and then upregulated vascular endothelial growth factor (VEGF) and angiopoietin 2(ANGPT2), whereas knockdown of KPNA2 inhibited STAT3 phosphorylation and then downregulated VEGF and ANGPT2. Conclusion: Our study demonstrates that hypoxia promotes the binding of STAT3 to KPNA2 and KPNA2 promotes angiogenesis under hypoxia by promoting the binding of STAT3 and JAK1 and regulating STAT3 phosphorylation. [ABSTRACT FROM AUTHOR]