贵州蕨类植物一新记录种——鳞蕗蕨

报道了贵州蕨类植物一新记录种--鳞蕗蕨[Mecodium levingei (Clarke) Cop.]     

Lomagramma yunnanensis Ching, a new synonym from China

报道了广西蕨类植物一新记录属--藤蕨科网藤蕨属Lomagramma J.Sm.;经野外观察及标本研究,将云南网藤蕨L.yunnanensis Ching处理为网藤蕨L.matthewii(Ching)Holttum的异名,并绘制了墨线图以便于分类识别.     

云南凤尾蕨属一新种

凤尾蕨属一新种-菜阳河凤尾蕨(Pteris caiyangheensis L.L.Deng sd.nov.).     

中国肿足蕨科一新记录属——翼囊蕨属（英文）

报道了中国肿足蕨科一新记录属——翼囊蕨属(Didymochlaena Desv.)。该属为泛热带分布的单型属,在中国为首次记录。本文结合原始文献对该属及其折囊蕨种的特征进行了详细描述。     

贵州蕨类植物一新记录属——乌木蕨属Blechnidium Moore

本文报道了贵州蕨类植物一新记录属——乌木蕨属Blechnidium Moore,该属为乌毛蕨科Blechnaceae一单种属,仅乌木蕨Blechnidium melanopus（Hook.）Moore一种。此物种分布区狭窄,数量有限,在贵州的发现对研究其地理与区系很有意义。     

贵州蕨类植物一新记录属——乌木蕨属

报道了贵州蕨类植物一新记录属——乌木蕨属(Blechnidium Moore),该属为乌毛蕨科(Blechnaceae)一单种属,仅乌木蕨[Blechnidium melanopus(Hook.)Moore]1种。此物种分布区狭窄,数量有限,在贵州的发现对研究其地理与区系很有意义。     

中国网藤蕨属一新异名

报道了广西蕨类植物一新记录属——藤蕨科网藤蕨属LomagrammaJ.Sm.;经野外观察及标本研究,将云南网藤蕨L.yunnanensis Ching处理为网藤蕨L.matthewii(Ching)Holttum的异名,并绘制了墨线图以便于分类识别。     

耳蕨属一新组——新生耳蕨组

描述了耳蕨属一新组——新生耳蕨组Sect．Neopolystichum Ching。小羽片背面具披针形小鳞片 使得新生耳蕨组显著区别于后生耳蕨组Sect．Metapolystichum Tagawa(emend．Zhang＆Kung,1996)。 本文对新生耳蕨组进行了分类学研究,共记载本组植物7种,并给出了各种植物的地理分布。认为九州 耳蕨P．kiusiuense Tagawa是大叶耳蕨P．grandifrons C. Chr．的一异名,二尖耳蕨P.biaristatum(Bl．)Moore极有可能并不分布于喜马拉雅、中南半岛、缅甸和云南。     

中国蹄盖蕨科安蕨属一新记录杂交种——华日安蕨

报道了采自安徽省祁门县安凌镇的中国蹄盖蕨科安蕨属一新记录植物——华日安蕨(Anisocampium×saitoanum (Sugim.) M. Kato)。推测该植物是华东安蕨(A. sheareri (Baker) Ching)与日本安蕨(A. niponicum(Mett.) Yea C. Liu,W. L. Chiou et M. Kato)的自然杂交种,形态介于两亲本之间。对华日安蕨的形态特征进行了描述,并提供了墨线图和安蕨属植物分类检索表。     

河南省鳞毛蕨科耳蕨属一新记录种——亮叶耳蕨

报道了河南省鳞毛蕨科耳蕨属一新记录种——亮叶耳蕨(Polystichum lanceolatum Baker)。对该种进行了特征描述,并编制了河南耳蕨属植物检索表。该种近似正宇耳蕨(P.liui Ching),但羽片上侧耳状凸起不明显,边缘有7～8个具短刺头的牙状齿,孢子囊群在主脉上侧最多3个,下侧不育或偶有1个,囊群盖圆盾形,全缘等特征而不同。凭证标本存放于河南农业大学植物标本馆(HEAC)。     

广东蕨类植物新资料

报道了2个新异名,1个新等级和35种蕨类植物在广东的分布新记录。正安肋毛蕨（Ctenitis changanensis Ching）和信宜铁角蕨（Asplenium xinyiense Ching et S.H.Wu）分别作直鳞肋毛蕨（Ctenitis eatoni (Bak.) Ching）和厚叶铁角蕨（Asplenium griffithianum Hook）的异名处理;齿翅井栏凤尾蕨（Pteris serralata（Miau）Y. H. Yan）被提升到种的等级;假芒萁属（Sticherus Presl）、柄盖蕨属（Peranema D. Don）、蛾眉蕨属（Lunathyrium Koidz.）和革舌蕨属（Scleroglossum Alderw）等4个属为广东分布新记录,小笠原卷柏（Selaginella boninensis Baker）为中国大陆分布新记录。广东现有蕨类已达到56科144属502种。     

地豆蔻属——中国姜科一新记录属

姜科地豆蔻属Elettariopsis Bak,是一个小属,分布于东南亚,我国尚无记录,最近在广西西南部石灰岩地区的林中见到1种,过去它被放在豆蔻属Amomum Roxb.中,现转移到此属。     

Doughnuts,daisy chains and crescent moons: the quest for the elusive apoptotic pore

How the two killer proteins Bax and Bak form the putative “apoptotic pore” that is responsible for irrevocably damaging mitochondria leading to cell death during apoptosis is considered the “holy grail” of apoptosis research. Indeed, even whether Bax and Bak form a pore remains contentious largely due to the failure to detect such structures in cells or mitochondria. Two new super‐resolution microscopy studies in this issue of The EMBO Journal now provide tantalising evidence of ring‐like “apoptotic pores” on mitochondria of dying cells and provide new insight into how Bax and Bak bring about a cell's demise.     

A New Fungal Diterpene Induces VDAC1-dependent Apoptosis in Bax/Bak-deficient Cells

The pro-apoptotic Bax and Bak proteins are considered central to apoptosis, yet apoptosis occurs in their absence. Here, we asked whether the mitochondrial protein VDAC1 mediates apoptosis independently of Bax/Bak. Upon screening a fungal secondary metabolite library for compounds inducing apoptosis in Bax/Bak-deficient mouse embryonic fibroblasts, we identified cyathin-R, a new cyathane diterpenoid compound able to activate apoptosis in the absence of Bax/Bak via promotion of the VDAC1 oligomerization that mediates cytochrome c release. Diphenylamine-2-carboxilic acid, an inhibitor of VDAC1 conductance and oligomerization, inhibited cyathin-R-induced VDAC1 oligomerization and apoptosis. Similarly, Bcl-2 overexpression conferred resistance to cyathin-R-induced apoptosis and VDAC1 oligomerization. Silencing of VDAC1 expression prevented cyathin-R-induced apoptosis. Finally, cyathin-R effectively attenuated tumor growth and induced apoptosis in Bax/Bak-deficient cells implanted into a xenograft mouse model. Hence, this study identified a new compound promoting VDAC1-dependent apoptosis as a potential therapeutic option for cancerous cells lacking or presenting inactivated Bax/Bak.     

山西蕨类植物新资料

报道了山西省新记录的蕨类植物6种1变种,隶属6科、7属,它们是井栏边草、东方狗脊、贵阳铁角蕨、雅致针毛蕨、沼泽蕨、毛轴假蹄盖蕨和高大耳蕨.     

Reconstitution and Engineering of Apoptotic Protein Interactions on the Bacterial Cell Surface

The interactions between pro- and anti-apoptotic members of the Bcl-2 class of proteins control whether a cell lives or dies, and the study of these protein-protein interactions has been an area of intense research. In this report, we describe a new tool for the study and engineering of apoptotic protein interactions that is based on the flow cytometric detection of these interactions on the surface of Escherichia coli. After validation of the assay with the well-studied interaction between the Bak(72-87) peptide and the anti-apoptotic protein Bcl-x_L, the effect of both increasing and decreasing Bak peptide length on Bcl-x_L binding was investigated. Previous work demonstrated that the Bak(72-87) peptide also binds to the anti-apoptotic protein Bcl-2, albeit with lower binding affinity compared to Bcl-x_L. Here, we demonstrate that a slightly longer Bak peptide corresponding to amino acids 72-89 of Bak binds Bcl-x_L and Bcl-2 equally well. Approximate binding affinity calculations on these peptide-protein complexes confirm the experimental observations. The flow cytometric assay was also used to screen a saturation mutagenesis library of Bak(72-87) variants for improved affinity to Bcl-x_L. The best variants obtained from this library exhibit an apparent K_d to Bcl-x_L 4-fold lower than that of wild-type Bak(72-87).     

Disruption of the VDAC2–Bak interaction by Bcl-xS mediates efficient induction of apoptosis in melanoma cells

The proapoptotic B-cell lymphoma (Bcl)-2 protein Bcl-x_S encloses the Bcl-2 homology (BH) domains BH3 and BH4 and triggers apoptosis via the multidomain protein Bak, however, the mechanism remained elusive. For investigating Bcl-x_S efficacy and pathways, an adenoviral vector was constructed with its cDNA under tetracycline-off control. Bcl-x_S overexpression resulted in efficient apoptosis induction and caspase activation in melanoma cells. Indicative of mitochondrial apoptosis pathways, Bcl-x_S translocated to the mitochondria, disrupted the mitochondrial membrane potential and induced release of cytochrome c, apoptosis-inducing factor and second mitochondria-derived activator of caspases. In melanoma cells, Bcl-x_S resulted in significant Bak activation, and Bak knockdown as well as Bcl-x_L overexpression abrogated Bcl-x_S-induced apoptosis, whereas Mcl-1 (myeloid cell leukemia-1) knockdown resulted in a sensitization. With regard to the particular role of voltage-dependent anion channel 2 (VDAC2) for inhibition of Bak, we identified here a notable interaction between Bcl-x_S and VDAC2 in melanoma cells, which was proven in reciprocal coimmunoprecipitation analyses. On the other hand, Bcl-x_S showed no direct interaction with Bak, and its binding to VDAC2 appeared as also independent of Bak expression. Suggesting a new proapoptotic mechanism, Bcl-x_S overexpression resulted in disruption of the VDAC2–Bak interaction leading to release of Bak. Further supporting this pathway, overexpression of VDAC2 strongly decreased apoptosis by Bcl-x_S. New proapoptotic pathways are of principle interest for overcoming apoptosis deficiency of melanoma cells.     

Mitochondrial apoptosis induced by BH3‐only molecules in the exclusive presence of endoplasmic reticular Bak

Bak and Bax are critical apoptotic mediators that naturally localize to both mitochondria and the endoplasmic reticulum (ER). Although it is generally accepted that mitochondrial expression of Bak or Bax suffices for apoptosis initiated by BH3‐only homologues, it is currently unclear whether their reticular counterparts may have a similar potential. In this study, we show that cells exclusively expressing Bak in endoplasmic membranes undergo cytochrome c mobilization and mitochondrial apoptosis in response to BimEL and Puma, even when these BH3‐only molecules are also targeted to the ER. Surprisingly, calcium was necessary but not sufficient to drive the pathway, despite normal ER calcium levels. We provide evidence that calcium functions coordinately with the ER‐stress surveillance machinery IRE1α/TRAF2 to transmit apoptotic signals from the reticulum to mitochondria. These results indicate that BH3‐only mediators can rely on reticular Bak to activate an ER‐to‐mitochondria signalling route able to induce cytochrome c release and apoptosis independently of the canonical Bak,Bax‐dependent mitochondrial gateway, thus revealing a new layer of complexity in apoptotic regulation.     

Translocation of a Bak C-terminus mutant from cytosol to mitochondria to mediate cytochrome C release: implications for Bak and Bax apoptotic function

Background

One of two proapoptotic Bcl-2 proteins, Bak or Bax, is required to permeabilize the mitochondrial outer membrane during apoptosis. While Bax is mostly cytosolic and translocates to mitochondria following an apoptotic stimulus, Bak is constitutively integrated within the outer membrane. Membrane anchorage occurs via a C-terminal transmembrane domain that has been studied in Bax but not in Bak, therefore what governs their distinct subcellular distribution is uncertain. In addition, whether the distinct subcellular distributions of Bak and Bax contributes to their differential regulation during apoptosis remains unclear.

Methodology/Principal Findings

To gain insight into Bak and Bax targeting to mitochondria, elements of the Bak C-terminus were mutated, or swapped with those of Bax. Truncation of the C-terminal six residues (C-segment) or substitution of three basic residues within the C-segment destabilized Bak. Replacing the Bak C-segment with that from Bax rescued stability and function, but unexpectedly resulted in a semi-cytosolic protein, termed Bak/BaxCS. When in the cytosol, both Bax and Bak/BaxCS sequestered their hydrophobic transmembrane domains in their hydrophobic surface groove. Upon apoptotic signalling, Bak/BaxCS translocated to the mitochondrial outer membrane, inserted its transmembrane domain, oligomerized, and released cytochrome c. Despite this Bax-like subcellular distribution, Bak/BaxCS retained Bak-like regulation following targeting of Mcl-1.

Conclusions/Significance

Residues in the C-segment of Bak and of Bax contribute to their distinct subcellular localizations. That a semi-cytosolic form of Bak, Bak/BaxCS, could translocate to mitochondria and release cytochrome c indicates that Bak and Bax share a conserved mode of activation. In addition, the differential regulation of Bak and Bax by Mcl-1 is predominantly independent of the initial subcellular localizations of Bak and Bax.