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CHITINASE LIKE1 Regulates Root Development of Dark-Grown Seedlings by Modulating Ethylene Biosynthesis in Arabidopsis thaliana

The plant hormone ethylene plays a regulatory role in development in light- and dark-grown seedlings. We previously isolated a group of small-molecule compounds with a quinazolinone backbone, which were named acsinones (for ACC synthase inhibitor quinazolinones), that act as uncompetitive inhibitors of 1-aminocyclopropane-1-carboxylic acid (ACC) synthase (ACS). Thus, the triple response phenotype, which consists of shortened hypocotyls and roots, radial swelling of hypocotyls and exaggerated curvature of apical hooks, was suppressed by acsinones in dark-grown (etiolated) ethylene overproducer (eto) seedlings. Here, we describe our isolation and characterization of an Arabidopsis revert to eto1 9 (ret9) mutant, which showed reduced sensitivity to acsinones in etiolated eto1 seedlings. Map-based cloning of RET9 revealed an amino acid substitution in CHITINASE LIKE1 (CTL1), which is required for cell wall biogenesis and stress resistance in Arabidopsis. Etiolated seedlings of ctl1ret9 showed short hypocotyls and roots, which were augmented in combination with eto1-4. Consistently, ctl1ret9 seedlings showed enhanced sensitivity to exogenous ACC to suppress primary root elongation as compared with the wild type. After introducing ctl1ret9 to mutants completely insensitive to ethylene, genetic analysis indicated that an intact ethylene response pathway is essential for the alterations in root and apical hook but not hypocotyl in etiolated ctl1ret9 seedlings. Furthermore, a mild yet significantly increased ethylene level in ctl1 mutants was related to elevated mRNA level and activity of ACC oxidase (ACO). Moreover, genes associated with ethylene biosynthesis (ACO1 and ACO2) and response (ERF1 and EDF1) were upregulated in etiolated ctl1ret9 seedlings. By characterizing a new recessive allele of CTL1, we reveal that CTL1 negatively regulates ACO activity and the ethylene response, which thus contributes to understanding a role for ethylene in root elongation in response to perturbed cell wall integrity

Hematopoietic stem cell transplantation in children with acute leukemia: similar outcomes in recipients of umbilical cord blood versus marrow or peripheral blood stem cells from related or unrelated donors

PurposeThis study compared outcomes in children with acute leukemia who underwent transplantations with umbilical cord blood (UCB), bone marrow, or peripheral blood stem cells from a human leukocyte antigen (HLA)-matched related donor (MRD) or an unrelated donor (URD).MethodsThis retrospective study included consecutive acute leukemia patients who underwent their first allogeneic hematopoietic stem cell transplantation (HSCT) at Samsung Medical Center between 2005 and 2010. Patients received stem cells from MRD (n=33), URD (n=46), or UCB (n=41).ResultsNeutrophil and platelet recovery were significantly longer after HSCT with UCB than with MRD or URD (P<0.01 for both). In multivariate analysis using the MRD group as a reference, the URD group had a significantly higher risk of grade III to IV acute graft-versus-host disease (GVHD; relative risk [RR], 15.2; 95% confidence interval [CI], 1.2 to 186.2; P=0.03) and extensive chronic GVHD (RR, 6.9; 95% CI, 1.9 to 25.2; P<0.01). For all 3 donor types, 5-year event-free survival (EFS) and overall survival were similar. Extensive chronic GVHD was associated with fewer relapses (RR, 0.1; 95% CI, 0.04 to 0.6; P<0.01). Multivariate analysis showed that lower EFS was associated with advanced disease at transplantation (RR, 3.2; 95% CI, 1.3 to 7.8; P<0.01) and total body irradiation (RR, 2.1; 95% CI, 1.0 to 4.3; P=0.04).ConclusionSurvival after UCB transplantation was similar to survival after MRD and URD transplantation. For patients lacking an HLA matched donor, the use of UCB is a suitable alternative

Efficacy of Itraconazole Prophylaxis for Autologous Stem Cell Transplantation in Children with High-Risk Solid Tumors: A Prospective Double-Blind Randomized Study

∙ The authors have no financial conflicts of interest. Purpose: The risk of invasive fungal infection is greater for allogeneic hematopoietic stem cell transplantation (HSCT) than for autologous transplantation. Therefore, many transplantation centers use antifungal prophylaxis for allogeneic HSCT, however, there exists no standard guidelines or consensus regarding autologous HSCT. Materials and Methods: A prospective double-blind randomized study was conducted in autologous HSCT recipients who were divided into prophylaxis and empirical treatment groups, and we investigated the efficacy of itraconazole prophylaxis in pediatric autologous HSCT. Results: Total 87 autologous HSCT episodes in 55 children with high-risk solid tumors were studied. No invasive fungal infections occurred in either group. However, patients in the prophylaxis group had a significantly shorter duration of fever (p &lt; 0.05) and received antibacterial treatment of shorter duration (p &lt; 0.05) with fewer numbers of antibiotics (p &lt; 0.05 for the use of second line antibiotics) than those in the empirica

The Role of Bec1/CtBP1 complex in Regulation of RE1/NRSE-Containing Gene Expression in Neuronal Gene Differentiation and Huntington’s disease

漢丁頓舞蹈症是一種遺傳性的神經退化性疾病，主要的特徵是由REST/NRSF所調控的基因轉錄受到抑制，導致紋狀體的神經細胞大量死亡。REST/NRSF是一個抑制型轉錄因子，會與啟動子上一段含有23個鹼基對的保守序列RE1/NRSE結合，藉此在胚胎幹細胞、未分化的神經先驅幹細胞及非神經細胞中，抑制與許多神經有關的基因表現。REST/NRSF會招募許多輔助抑制物，包括C端結合蛋白CtBP1， 而形成一個新奇複合物，藉此執行抑制的功能。我們實驗室先前從GCH-1的顯性負面調控機制中，鑑定了一個新奇基因Bec1。Bec1的C端有一個保守的YTH區域，此保守區域曾被證明具有與RNA結合及ATP水解酶的能力。在我們的研究中，我們發現Bec1會藉由與CtBP1結合，來誘導某些含有RE1/NRSE序列的基因表現，例如：SCG10、BDNF。同時，Bec1的YTH區域對於Bec1及CtBP1兩者間結合是很重要的。另外，我們實驗室之前的實驗結果顯示Bec1在R6/2老鼠中，其表現量會降低，而我們的實驗結果也發現突變的Huntingtin會減少細胞中可溶解的Bec1蛋白質。Bec1蛋白質表現量的降低可能也是造成在漢丁頓舞蹈症中含有RE1/NRSE序列的基因表現受到抑制的原因之一。Huntington’s disease is an inherited neurodegenerative disease characterized by the repression of REST/NRSF target gene transcription, leading to large amounts of neuron death in the striatum. REST/NRSF is a silencing transcription factor binding to a consensus 23bp DNA sequence in promoter, RE1/NRSE, to restrict neural gene expression in embryo stem cells, undifferentiated neuronal progenitor and non-neuronal cells. REST/NRSF recruits a lot of corepressor, including a C-terminal binding protein, CtBP1, and forms a novel corepressor complex, to exert repression activity. Our lab previously identified a novel gene, Bec1, from the GCH-1 dominant negative cell models. The C-terminal of Bec1, a conserved YTH domain, has been recorded having RNA-binding and ATPase ability. In our study, we discovered that Bec1 can induce some RE1/NRSE-containing gene expression, such as SCG10 and BDNF, through interaction with CtBP1. Meanwhile, the YTH domain of Bec1 is important for Bec1 and CtBP1 interaction. Furthermore, our lab previously shows that Bec1 is reduced in R6/2 mice and our data also are found that mutant Htt reduces soluble Bec1 in cells. The reduction of Bec1 might be a reason for RE1/NRSE gene repression in HD.Contents試委員審定書 i謝 ii文摘要 iiinglish Abstract ivbbrevation vhapter1 Introduction 1.1 The role of REST/NRSF during neuronal development 1.2 The corepressor CtBP 5.3 The novel gene Bec1 and its known function 6.4 Huntington’s disease 9hapter2 Materials and Methods 14.1 Plasmid constructions 14.1.1 Luciferase Reporter gene constructs 14.1.2. siRNA constructs for REST/NRSF gene suppression 15.1.3. Dominant-negative NRSF 16.1.4. CtBP expression constructs 16.1.5. Full-length, deleted and mutant form of Bec1 expression constructs 16.1.6. PolyQ constructs 17.2 STHdHQ7 and STHdHQ109 cell 18.3 Cell culture and transient transfection 18.4 R6/2 mice 19.5 Luciferase assay 19.6 RT-PCR 19.7 Immunofluorescence staining 20.8 Chromatin immunoprecipitation (ChIP 21.9 GST and His tagged protein induction 22.10 GST-pull down assay 22.11 Western blotting 23.12 Separation of protein soluble fractions and precipitates 24hapter 3 Results 25.1 RE1/NRSE is a silencer of SCG10 promoter and represses SCG10 expression by REST/NRSF repressive complex mediation 25.1.1 The RE1/NRSE regulates SCG10 expression in REST/NRSF+ cell in vitro 25.1.2 Silencing of REST/NRSF by a siRNA strategy results in an increase of SCG10 transcription in REST/NRSF+ cell in vitro and in vivo 26.1.3 Overexpression of dominant-negative NRSF (dn NRSF) reverses REST/ NRSF-mediated SCG10 suppression in vitro 27.1.4 SCG10 is silenced through histone modification not by DNA methylation 27.2 Bec1 promotes RE1/NRSE-containing gene expression 28.2.1 Bec1 induces SCG10 expression in vitro 28.2.2 Repression of neuronal gene expression is disrupted by Bec1 in vivo 29.3 Bec1 increases some neural-specific genes expression by impairing the REST/NRSF repression system 30.4 Interaction of Bec1 and CtBP1 is a possible mechanism for RE1/NRSE-containing gene derepression 31.4.1 Subcellular localization of Bec1 in HeLa cell 31.4.2 Subcellular localization of CtBP1 in HeLa cel 31.4.3 Interaction of Bec1 and CtBP1 32.4.4 Bec1 interacts with CtBP1 by C-terminal domain 32.4.5 Bec1 and CtBP1 interact directly in vitro, and YTH domain of Bec1 is significant in this event 33.5 The protein level of Bec1 is reduced in STHdHQ7and STHQ109cells during neural differentiation 34.6 81Q-Htt facilitates aggregate formation of Bec1 35hapter 4 Discussion 36.1 Bec1 is a novel gene involved in neural differentiation 36.2 Bec1 induces neuronal gene expression by derepressing REST/NRSF repressive complex 37.3 Bec1-CtBP1 interaction is a possible mechanism for REST/NRSF repressive complex disruption 38.4 YTH domain of Bec1 is significant for CtBP1 binding and RE1/NRSE-containing gene induction 39.5 Bec1 is aggregated by mutant Htt and lost its function in R6/2 mice 40.6. Bec1 is aggregated by mutant Htt and lost its function in R6/2 mice 41hapter 5 Reference 43hapter 6 Figures and Tables 55igure 1. Repression of SCG10 expression by REST/NRSF 55igure 2. Induction of SCG10 Expression by dnNRSF or siNRSF in vitro 56igure 3. Induction of SCG10 by Bec1 in vivo 57igure 4. Induction of SCG10 by Bec1 and d200 in vitro 58igure 5. Induction of SCG10 by Bec1 in vivo 59igure 6. Induction of SCG10 expression by interfering REST /NRSF repressive complex in vivo 60igure 7. Immunofluorescence staining of co-localization of Bec1 and CtBP1 61igure 8. Interaction of Bec1 and CtBP1 by GST-pull down assay analysis 62igure 9. Direct interaction of Bec1 and CtBP1 63igure 10. Direct interaction of Bec1 and CtBP1 64igure 11. Reduction of proteins level of Bec1 in STHdHQ7 and STHdHQ109 cells during neural differentiation 65igure 12. Promotion of Bec1 aggregation by 81Q-Htt 66able 1. Plasmid constructs used in our study 67able 2. Primers used in RT-PCR 68hapter 7 Appendix 69ppendix 1. NRSE/RE1 sequences in neural-specific gene 69ppendix 2. Model of NRSE/RE1 dependent NRSF/REST repressive complex 70ppendix 3. Reduction of Bec1 in R6/2 mice 71ppendix 4. Amino acid sequence and possible functional domain of Bec1 72ppendix 5. Involvement of Bec1 in cholinergic neuron differentiation 73ppendix 6.The corepressors role of CtBP in REST/NRSF repressive complex 7