木立芦荟小孢子母细胞减数分裂与花粉育性关系的初步研究

文章从减数分裂过程、小孢子发育两方面,探讨了木立芦荟（Aloe arboresens Mill.）花粉败育的原因。木立芦荟花粉母细胞染色体数目为2n=14,由四对长染色体和三对短染色体组成,属二型性核型。其减数分裂异常,发现存在单价体和多价体、染色体桥、落后染色体、不均等分离、微核等。同时观察到木立芦荟染色体具有极度的粘质性,使减数分裂各阶段的染色体不易散开。统计各种异常现象出现的频率并分析了这些异常现象形成的可能机制及对正常小孢子形成的影响,推测染色体间的丝状粘连可能是木立芦荟小孢子母细胞减数分裂异常并导致败育花粉产生的主要因素。成熟花粉粒中90%以上为败育花粉,属碘败型。     

小胡杨花粉母细胞减数分裂染色体行为研究

采用常规压片法对小胡杨花粉母细胞减数分裂过程染色体行为及花粉特性进行了研究.结果表明:小胡杨花粉母细胞减数分裂过程中表现出极强的异质性,减数分裂各时期异常细胞出现率均超过70%.其中,终变期存在大量单价体、后期观察到落后染色体,证明小胡杨的两个亲本亲缘关系较远.小胡杨花粉母细胞减数分裂过程高频率异常现象(后期I落后染色体71.87%,染色体桥8.13%;末期Ⅰ有77.18%的微核细胞;后期Ⅱ有85.60%的异常细胞等)的发生直接导致其大部分花粉发育异常(99.48%),表现出远缘杂种的败育特性.     

黄花烟草单倍体植株花粉粒败育的观察

甘肃黄花烟草未授粉子房培养的愈伤组织再生的单倍体植株(2n:2x=24),生长矮小,叶片和花也较小。花粉粒有两种类型:小型直径平均17.41微米,大型直径平均42.37微米,都无沟槽和萌发孔,外壁雕纹显著增厚。二倍体植株正常花粉粒直径平均26.28微米。根据单倍体植株花粉粒败育过程的细胞学观察,约80%的花粉母细胞减数分裂正常,形成四分体,进一步发育成小型的单核花粉粒;但停滞在单核阶段,不能进入有丝分裂,以致不能形成成熟的二核花粉粒;最后细胞核和细胞质解体消失,成为空壳的败育花粉粒。另外的20%的花粉母细胞,由于1—2个落后染色体的存在,减数分裂不能正常进行,变为一种大型的四核花粉粒;最后细胞核和细胞质解体消失,成为空壳的败育花粉粒。     

百合花粉母细胞减数分裂异常现象观测分析

对“Siberia”百合小孢子母细胞减数分裂异常进行了系统的细胞学观察,发现“Siberia”百合小孢母细胞减数分裂中存在不等二价体、倒位环、染色体桥、滞后染色体、微核、不均等分离、染色体显著减少的核、游离核、异常四分体、无核花粉等异常现象。研究表明：“Siberia”百合长期进行无性繁殖引起染色体结构变异,导致减数分裂异常,小孢子母细胞减数分裂异常是导致花粉败育的主要原因。     

高羊茅花粉母细胞减数分裂及其雄性不育的细胞生理学研究

为探讨高羊茅雄性不育株A22013189的小孢子发育过程及其败育的生理学机理,以可育株189为对照,对其结实能力、花粉活力、花粉母细胞减数分裂进程中的染色体行为及生理生化特征进行研究。结果表明:(1)不育株A22013189花粉数量少,花粉粒空瘪皱褶,自交不结实,在杂交中作父本获得杂交后代的可能性极小。(2)从减数分裂前期Ⅰ至四分体时期,不育株A22013189花粉母细胞存在大量落后染色体、染色体桥和断片、微核、单价染色体、不均等分离、染色体分裂不同步、游离染色体、三分体、60°纺锤体、染色体缺失等异常现象,初步分析这些小孢子异常分裂是导致高羊茅花粉败育的细胞学原因之一。(3)不育株A22013189的可溶性蛋白质、可溶性糖含量在整个发育时期都显著低于同期可育株189;苗期至造孢细胞期,A22013189游离脯氨酸含量与可育株189无显著差异,但减数分裂期至花粉成熟期,A22013189游离脯氨酸含量却显著低于同期可育株189;苗期至造孢细胞期,A22013189丙二醛含量显著低于同期可育株189,但小孢子进入减数分裂期后,A22013189丙二醛的增加速度和积累量明显高于同期可育株189。研究发现,高羊茅雄性不育株花粉母细胞减数分裂染色体行为异常,生长发育过程存在物质能量代谢降低,有害物质积累现象。研究结果对于高羊茅败育机理研究及杂交育种亲本选择有重要的理论指导意义。     

长春蒲公英雄性不育株形态学观察与败育细胞学研究

在长春蒲公英(Taraxacum junpeianum Kitam.)株群中发现雄性不育现象,为研究其败育机理及特点,探寻其不育基因,采用形态观察法、石蜡切片技术和染色体压片法,对长春蒲公英野生型及其雄性不育株的花药发育过程和花粉母细胞减数分裂过程进行了观察。结果表明:(1)长春蒲公英雄性不育株花药中部发红、干瘪、无花粉散出。与野生型比较,雄性不育株雄蕊更短,子房更窄,种子形态更加狭长;(2)长春蒲公英雄性不育株败育时期为四分体到单核小孢子前期,败育方式为小孢子自身异常发育,绒毡层异常分解,互相粘连败育;(3)长春蒲公英雄性不育株花粉母细胞减数分裂二分体时期出现落后微核,随后产生极少四分体,并且四分体产生大量染色体桥,小孢子营养物质流失,彻底败育。因此,长春蒲公英雄性不育株败育彻底、稳定,并且有种的特点。小孢子自身异常发育和绒毡层异常分解是导致败育的主要原因。     

甘蔗-滇蔗茅杂交F_1花粉母细胞减数分裂过程GISH分析

研究甘蔗属与滇蔗茅属间远缘杂交F1染色体遗传行为具有重要科学意义,可为发掘利用滇蔗茅野生优异基因资源提供细胞学依据。本研究采用常规压片技术对可育父本及不育杂交F1花粉母细胞减数分裂过程进行比较观察,结果显示可育父本云南95-19减数分裂正常,而不育杂交F1分裂异常;进一步对F1花粉母细胞减数分裂过程进行基因组荧光原位杂交(GISH,genome in situ hybridization)分析,结果表明:滇蔗茅与甘蔗属热带种的亲缘关系较远,双亲染色体在F1细胞中不能进行同源配对,终变期,15条滇蔗茅染色体以单价体形式存在,花粉母细胞减数分裂细胞中存在滞后染色体、染色体丢失和不均衡分离现象。甘蔗-滇蔗茅属间远缘杂交F1花粉母细胞减数分裂异常因而杂交F1花粉完全败育。     

紫斑牡丹栽培品种小孢子发育过程的细胞遗传学研究

本文对紫斑牡丹栽培品种的花平细胞减数分裂过程进行了系统研究,结果发现紫斑牡丹品种约６８．９６％的花平细胞在减数分裂过程表现正常,约有３１．０４％的花粉母细胞在减数分裂的比线期、中期Ⅰ、后期Ⅰ、中期Ⅱ、后期Ⅱ及四分体时期观察到染色体行为异常。本实验表明,在小孢子形成过程中,多数小孢子发育政党,但有约３１．０４％的花粉母细胞减数分裂异常,导致了花粉的败育。     

OT杂种系百合品种‘Cocossa’小孢子败育细胞学研究

以OT百合‘Cocossa’为材料,采用醋酸洋红染色烤片法和石蜡切片法,对该品种花粉母细胞减数分裂过程以及绒毡层在花粉母细胞发育过程中的变化进行系统的细胞学观察。研究发现:(1)当百合花蕾长度在2.5~4.5 cm时,花粉母细胞处在减数分裂时期。(2)在花粉母细胞减数分裂的过程中,出现了较多染色体异常现象:中期Ⅰ出现染色体环;后期Ⅰ出现了滞后染色体和染色体桥;在末期Ⅰ和末期Ⅱ细胞出现不均等分裂和微核;处于同一花蕾和同一花药的花粉母细胞减数分裂具有不同步性,能同时观察到2个不同时期的分裂相;形成畸形、无核、多核的异常小孢子。(3)在末期Ⅱ和单核花粉粒时期,绒毡层延迟降解,引起多核花粉粒、畸形花粉粒以及花粉粒自溶现象。结果表明:OT百合‘Cocossa’小孢子败育是花粉母细胞异常减数分裂与绒毡层异常降解共同导致的。     

兰州百合小孢子母细胞减数分裂异常现象的观察

对兰州百合(Lilium davidii var.unicolor)小孢子母细胞减数分裂异常进行了研究,发现存在不等二价体、同源染色体早分离、染色体桥、不均等分离、滞后染色体、核外染色体、微核等。分析了这些异常形成的可能机制及对正常小孢子形成的影响。人工花粉萌发实验表明：小孢子母细胞减数分裂异常是导致花粉败育的主要原因。认为兰州百合长期行无性繁殖引起染色体结构变异,导致减数分裂异常。     

A Unique Protease Cleavage Site Predicted in the Spike Protein of the Novel Pneumonia Coronavirus (2019-nCoV) Potentially Related to Viral Transmissibility

正Dear Editor,In December 2019, a novel human coronavirus caused an epidemic of severe pneumonia(Coronavirus Disease 2019,COVID-19) in Wuhan, Hubei, China(Wu et al. 2020; Zhu et al. 2020). So far, this virus has spread to all areas of China and even to other countries. The epidemic has caused 67,102 confirmed infections with 1526 fatal cases     

Curcuminoids as inhibitors of thioredoxin reductase: A receptor based pharmacophore study with distance mapping of the active site

Curcumin is the yellow pigment of turmeric that interacts irreversibly forming an adduct with thioredoxin reductase (TrxR), an enzyme responsible for redox control of cell and defence against oxidative stress. Docking at both the active sites of TrxR was performed to compare the potency of three naturally occurring curcuminoids, namely curcumin, demethoxy curcumin and bis-demethoxy curcumin. Results show that active sites of TrxR occur at the junction of E and F chains. Volume and area of both cavities is predicted. It has been concluded by distance mapping of the most active conformations that Se atom of catalytic residue SeCYS498, is at a distance of 3.56 from C13 of demethoxy curcumin at the E chain active site, whereas C13 carbon atom forms adduct with Se atom of SeCys 498. We report that at least one methoxy group in curcuminoids is necessary for interation with catalytic residues of thioredoxin. Pharmacophore of both active sites of the TrxR receptor for curcumin and demethoxy curcumin molecules has been drawn and proposed for design and synthesis of most probable potent antiproliferative synthetic drugs.     

Comparative morphology of the carpel in the Liliaceae: Hewardieae, Petrosavieae, and Tricyrteae

The young pistils in the melanthioid tribes, Hewardieae, Petrosavieae and Tricyrteae, are uniformly tricarpellate and syncarpous. They lack raphide idioblasts. All are multiovulate, with bitegmic ovules. The Petrosavieae are marked by the presence of septal glands and incomplete syncarpy. Tepals and stamens adhere to the ovary in the Hewardieae and the Petrosavieae but not in the Tricyrteae. Two vascular bundles occur in the stamens of the Hewartlieae and Tricyrtis latifolia. Ventral bundles in the upper part of the ovary of the Hewardieae are continuous with compound septal bundles and placental bundles in the lower part. Putative ventral bundles occur in the alternate position in the Tricyrteae and putative placental bundles in the opposite. position in the Petrosavieae. The dichtomously branched stigma in each carpel of the Tricyrteae is supplied by a bifurcated dorsal bundle.     

Enterovirus 71 3C proteolytically processes the histone H3 N-terminal tail during infection

Highlights
1. The N-terminal tail of histone H3 is specifically cleaved during EV71 infection.
2. Viral protease 3C is identified as a protease responsible for proteolytically processing the N-terminal H3 tail.
3. Our finding reveals a new epigenetic regulatory mechanism for Enterovirus 71 in virus-host interactions.     

Detection of EBV and HHV6 in the Brain Tissue of Patients with Rasmussen’s Encephalitis

Rasmussen’s encephalitis (RE) is a rare pediatric neurological disorder, and the exact etiology is not clear. Viral infection may be involved in the pathogenesis of RE, but conflicting results have reported. In this study, we evaluated the expression of both Epstein-Barr virus (EBV) and human herpes virus (HHV) 6 antigens in brain sections from 30 patients with RE and 16 control individuals by immunohistochemistry. In the RE group, EBV and HHV6 antigens were detected in 56.7% (17/30) and 50% (15/30) of individuals, respectively. In contrast, no detectable EBV and HHV6 antigen expression was found in brain tissues of the control group. The co-expression of EBV and HHV6 was detected in 20.0% (6/30) of individuals. In particular, a 4-year-old boy had a typical clinical course, including a medical history of viral encephalitis, intractable epilepsy, and hemispheric atrophy. The co-expression of EBV and HHV6 was detected in neurons and astrocytes in the brain tissue, accompanied by a high frequency of CD8⁺ T cells. Our results suggest that EBV and HHV6 infection and the activation of CD8⁺ T cells are involved in the pathogenesis of RE.     

Perinatal Vertical Transmission of Chikungunya Virus in Ruili,a Town on the Border between China and Myanmar

正Dear Editor,Chikungunya virus (CHIKV), an arbovirus in the family of Togaviridae, genus Alphavirus, is transmitted by the A.aegyptii or A. albopictus mosquito, and causes disease in humans characterized by fever, rash, and arthralgia (Silva and Dermody 2017; Suhrbier 2019). It was first reported in 1953 in Tanzania, and caused only a few outbreaks and sporadic cases in Africa and Asia in last century. However, in the epidemic in 2004, CHIKV acquired mutations that conferred enhanced transmission by the A. albopictus mosquito(Schuffenecker et al. 2006). Since then, it has successively caused outbreaks in Africa, the Indian Ocean, South East Asia, the South America, and Europe (Zeller et al. 2016).