Exercise and genetic rescue of SCA1 via the transcriptional repressor Capicua

Spinocerebellar ataxia type 1 (SCA1) is a fatal neurodegenerative disease caused by expansion of a translated CAG repeat in Ataxin-1 (ATXN1). To determine the long-term effects of exercise, we implemented a mild exercise regimen in a mouse model of SCA1 and found a considerable improvement in survival accompanied by up-regulation of epidermal growth factor and consequential down-regulation of Capicua, which is an ATXN1 interactor. Offspring of Capicua mutant mice bred to SCA1 mice showed significant improvement of all disease phenotypes. Although polyglutamine-expanded Atxn1 caused some loss of Capicua function, further reduction of Capicua levels--either genetically or by exercise--mitigated the disease phenotypes by dampening the toxic gain of function. Thus, exercise might have long-term beneficial effects in other ataxias and neurodegenerative diseases.     

PI3Kgamma is a key regulator of inflammatory responses and cardiovascular homeostasis

Class I phosphoinositide 3-kinase (PI3K) signaling pathways regulate several important cellular functions, including cellular growth, division, survival, and movement. Class IB PI3K (also known as PI3Kgamma) links heterotrimeric GTP-binding protein-coupled receptors to these pathways. Activation of class IB PI3K results in the rapid synthesis of phosphatidylinositol-3,4,5-trisphosphate [PtdIns(3,4,5)P3] and its dephosphorylation product PtdIns(3,4)P2 in the plasma membrane. These two lipid messengers bind to pleckstrin homology domain-containing effectors that regulate a complex signaling web downstream of receptor activation. Characteristic features of this pathway are the regulation of protein kinases and the regulation of small guanosine triphosphatases that control cellular movement, adhesion, contraction, and secretion. Most of the ligands that activate class IB PI3K are involved in coordinating the body's response to injury and infection, and recent studies suggest that small molecule inhibitors of this enzyme may represent a novel class of anti-inflammatory therapeutic agents.     

Stem-cell homeostasis and growth dynamics can be uncoupled in the Arabidopsis shoot apex

The shoot apical meristem (SAM) is a collection of stem cells that resides at the tip of each shoot and provides the cells of the shoot. It is divided into functional regions. The central zone (CZ) at the tip of the meristem is the domain of expression of the CLAVATA3 (CLV3) gene, encoding a putative ligand for a transmembrane receptor kinase, CLAVATA1, active in cells of the rib meristem (RM), located just below the CZ. We show here that CLV3 restricts its own domain of expression (the CZ) by preventing differentiation of peripheral zone cells (PZ), which surround the CZ, into CZ cells and restricts overall SAM size by a separate, long-range effect on cell division rate.     

IL-2真核质粒对乳酸杆菌载体口蹄疫VP1 DNA疫苗猪体免疫反应的分子佐剂效应

为研究猪IL-2真核表达质粒对乳酸杆菌载体口蹄疫VP1 DNA疫苗(Lactobacillus acidophilusSFMD-1)猪体免疫的分子佐剂效应,通过RT-PCR方法从猪的肠系膜淋巴结克隆猪IL-2基因,基于pRc/CMV2载体,构建编码猪IL-2的真核表达质粒pCSIL2,以RT-PCR方法分析了该质粒转染PK15细胞以后的mRNA表达。结果显示预期的429 bp IL-2带仅出现在pCSIL2转染细胞。试验猪单独免疫L.acidophilusSFMD-1或者联合免疫pCSIL2质粒,后者能够增强FMDV-VP1特异的T细胞和B细胞反应,免疫后5周,单独免疫组和联合免疫组的抗体水平分别为1.50和1.66;免疫后6周,抗体水平分别上升到1.83和2.28;在T细胞增殖试验中,L.acidophilusSFMD-1单独免疫组和pCSIL2联合免疫组的刺激指数(SI)分别为2.00和2.70。结果表明,联合应用IL-2真核表达质粒是改进乳酸杆菌载体口蹄疫VP1 DNA疫苗免疫原性和效能的有效方法。     

Requirement for coronin 1 in T lymphocyte trafficking and cellular homeostasis

The evolutionarily conserved actin-related protein (Arp2/3) complex is a key component of actin filament networks that is dynamically regulated by nucleation-promoting and inhibitory factors. Although much is known about actin assembly, the physiologic functions of inhibitory proteins are unclear. We generated coronin 1-/- mice and found that coronin 1 exerted an inhibitory effect on cellular steady-state F-actin formation via an Arp2/3-dependent mechanism. Whereas coronin 1 was required for chemokine-mediated migration, it was dispensable for T cell antigen receptor functions in T cells. Moreover, actin dynamics, through a mitochondrial pathway, was linked to lymphocyte homeostasis.     

Fibroblast growth factor receptor is a portal of cellular entry for herpes simplex virus type 1

Herpes simplex virus type 1 (HSV-1) is a ubiquitous pathogen responsible for considerable morbidity in the general population. The results presented herein establish the basic fibroblast growth factor (FGF) receptor as a means of entry of HSV-1 into vertebrate cells. Inhibitors of basic FGF binding to its receptor and competitive polypeptide antagonists of basic FGF prevented HSV-1 uptake. Chinese hamster ovary (CHO) cells that do not express FGF receptors are resistant to HSV-1 entry; however, HSV-1 uptake is dramatically increased in CHO cells transfected with a complementary DNA encoding a basic FGF receptor. The distribution of this integral membrane protein in vivo may explain the tissue and cell tropism of HSV-1.     

Absence of TGF-beta receptors and growth inhibitory responses in retinoblastoma cells

The responses of retinoblastoma tumor cells and normal retinal cells to various growth inhibitory factors were examined. Whereas fetal retinal cells were highly sensitive to the antimitogenic effects of transforming growth factor beta 1 (TGF-beta 1), retinoblastoma tumor cell lines were all resistant to this factor. Binding assays and affinity labeling of these cells with radioiodinated TGF-beta 1 revealed that the cells did not have TGF-beta receptors. The retinoblastoma cells lacked the three affinity-labeled proteins of 65, 95, and 300 kilodaltons typically seen in human cell lines and thus differed from normal retinal cells and from other types of neuroectodermal tumors that display the normal pattern of receptors. Loss of TGF-beta receptors, which is a rare event among tumor cells, may represent one mechanism through which these cells escape from negative control and form retinoblastomas.     

Multiple roles of Arabidopsis VRN1 in vernalization and flowering time control

Arabidopsis VRN genes mediate vernalization, the process by which a long period of cold induces a mitotically stable state that leads to accelerated flowering during later development. VRN1 encodes a protein that binds DNA in vitro in a non-sequence-specific manner and functions in stable repression of the major target of the vernalization pathway, the floral repressor FLC. Overexpression of VRN1 reveals a vernalization-independent function for VRN1, mediated predominantly through the floral pathway integrator FT, and demonstrates that VRN1 requires vernalization-specific factors to target FLC.     

GCK家族蛋白激酶MoSOK1调控稻瘟病菌的生长发育与致病性

稻瘟病菌致病相关基因功能的研究有助于揭示其致病机理,为稻瘟病防治提供理论依据。本研究利用基因替换技术对稻瘟病菌SOK1同源基因(MoSOK1)进行了分析。MoSOK1编码GCK(germinal center kinase)家族的Ste20蛋白激酶,其与全蚀病菌中对应蛋白具有最高同源性。本研究表明,MoSOK1基因在附着胞分化关键期上调表达;与野生型菌株相比,MoSOK1基因缺失突变体菌落颜色加深,气生菌丝减少,生长速度变慢,产孢量下降,分生孢子萌发延迟,致病性降低。另外,交配实验表明,MoSOK1基因缺失突变体能够进行交配,但产子囊壳能力降低。本研究初步表明,MoSOK1基因参与稻瘟病菌生长发育和致病过程。     

Evidence of arrested silk growth in maize at high planting density using phenotypic and transcriptional analyses

Increasing the planting density is an effective way to increase the yield of maize(Zea mays L.), although it can also aggravate ovary apical abortion-induced bald tips of the ears, which might, in turn, reduce the yield. While the mechanism underlying the regulation of drought-related abortion in maize is well established,high planting density-related abortion in maize remains poorly understood. Therefore, the present study was designed to investigate the mechanism underlying the ovary apical ab...     

光质对立体浮盘培育烟苗叶片光合特性及根系生长的影响

为研究光质对立体浮盘培育烟苗叶绿体色素、光合响应和根系发育的影响,试验设置白光(对照)、红光、蓝光和LED光4个处理。结果表明:与其他光质比较,蓝光光质下烟苗叶绿素a含量显著(P0.05)提高16.13%~28.57%、叶绿素b显著提高30.00%~36.84%,此外,类胡萝卜素含量比红光光质下显著提高18.18%;不同光质条件下烟苗叶片最大净光合速率(Pmax)的大小关系为蓝光白光LED光红光,且蓝光光质下烟苗光饱和点最高;红蓝光质下,烟苗根系长度、根系表面积、根系平均直径和根系体积均显著(P0.05)增加,以蓝光下烟苗根系发育最好,其烟苗4叶1心时根系长度达98.11cm、根系表面积22.78cm2、根系平均直径0.74mm和根系体积0.42cm3。本研究结果表明,采用蓝光光质更适用于烤烟立体育苗,有利于培育壮苗。