云南罗平中三叠世意外裸鱼的再研究

意外裸鱼(Gymnoichthys inopinatus)于2010年由Tintori等首次记述并归入基干新鳍鱼类。依据在云南省曲靖地区罗平县大凹子村中三叠世关岭组二段发现的新材料,对意外裸鱼进行了补充描述,并重新讨论了其系统发育关系。在意外裸鱼的新标本上,可见其续骨前端很可能与关节骨相关节,并有确切无疑的单一辅上颌骨,表明意外裸鱼应为鲱亚部(Halecomorphi)鱼类。此外,意外裸鱼的体表无鳞、椎体未骨化、髓棘和髓弓的结构和排列方式以及牙齿和尾脉棘的形状都与金尾鱼超科鱼类(caturoids)一致。系统发育分析结果表明意外裸鱼属于金尾鱼超科的基干类群。之前金尾鱼类主要见于欧洲和北美的侏罗系,现在公认的金尾鱼超科鱼类主要包括Liodesmidae中的Liodesmus属和金尾鱼科(Caturidae)中的Caturus和Amblysemius两属。意外裸鱼的发现不仅使金尾鱼类的出现提前了40Ma,而且填补了我国相关材料的空缺。     

山西柳林孙家沟组锯齿龙类新材料及其分类学意义(英文)

记述了产自山西柳林县薛村镇附近上二叠统孙家沟组的锯齿龙类新材料,包括两个单独的上颌齿和一个保存有牙齿的不完整齿骨。这两颗上颌齿与柳林黄河龙(Huanghesaurus liulinensis)正型标本来自同一地点同一层位且大小相当,由于同一地点没发现过其他的锯齿龙类,推测它们是同种甚至可能是同一个体而且应归入黄河龙;然而在形态特征上这两颗牙齿与矮小三川龙(Sanchuansaurus pygmaeus)正型标本上的牙齿完全相同,可以归入三川龙。新发现的齿骨与矮小三川龙和薛村山西龙(Shansisaurus xuecunensis)正型标本产自同一地点,层位与三川龙相同,低于山西龙的层位,推测很可能也属于三川龙,但是也不排除属于山西龙的可能性;在形态特征上与黄河龙正型标本在齿骨及其下颌齿的形态特征上未见明显差异,可以归入黄河龙。由于柳林黄河龙与薛村山西龙头后骨骼特征也基本一致,认为柳林薛村仅有一个属种的锯齿龙,矮小三川龙和柳林黄河龙应为薛村山西龙的晚出同义名。     

Tetrapod Footprints From the Upper Carboniferous of China

We documented tetrapod footprints from Baode, Shanxi, China identified as aff. Dimetropus. These are the first record of carboniferous tetrapods from what was the North China block, a microplate isolated from the Pangean nucleus during the Carboniferous.     

Dinosaur Footprints from the Lower Cretaceous Sarten Member of the Mojado Formation at Cerro de Cristo Rey,Dona Ana County,New Mexico

Dinosaur tracks and swimming traces have been discovered at three localities in the latest Albian Sarten Member of the Mojado Formation, Bisbee Group (= “Anapra Sandstone”), at Cerro de Cristo Rey in Sunland Park, southernmost Dona Ana County, New Mexico. These localities preserve footprints of ornithopod (Caririchnium) and theropod (Magnoavipes) dinosaurs, ?reptilian swimming traces and possible tracks of an ankylosaurian dinosaur. The Sarten Member is of the latest Albian age, so the Cerro de Cristo Rey tracks are slightly younger than the well-known late Albian tracksites of northeastern New Mexico. At Cerro de Cristo Rey, the dominance of ornithopod tracks and absence of sauropod tracks fit regional patterns of late Albian-early Cenomanian track distribution consistent with North American extirpation of sauropods before the end of Albian time. The deltaic/coastal plain depositional setting of the Sarten Member is also remarkably similar to the track-bearing late Albian-Cenomanian sandstones of NE New Mexico, Oklahoma, Nebraska, and SE Colorado, which also have a tetrapod footprint ichnofacies dominated by ornithopod (Caririchnium) and theropod (Magnoavipes) tracks throughout the so-called “dinosaur freeway.”     

Corimbatichnus fernandezi: A cluster of fossil bee cells from the late cretaceous‐early tertiary of Uruguay

Corimbatichnus fernandezi n.igen, n. isp. is a cluster of fossil bee cells from the Uruguayan Late Cretaceous‐early Tertiary Asencio Formation. It is composed of rows of small excavated cells contained in paleosol peds. Cells have inner surfaces somewhat rough and are closed with loose material. Separation among cells is very thin, and the cells are orientated uniformly, showing a great economy of space as in some halictine constructions. Corimbatichnus can be distinguished from Rosellichnus and Uruguay by its convex face, excavated cells and the spatial arrangement of them.     

贵州寒武纪杷榔组古蠕虫类埋藏特征及意义*

贵州剑河寒武纪杷榔组辣子寨剖面含有丰度较高的古蠕虫类化石。化石鉴定为Wronascolex geyiensis, 主要保存在三个层位。在对三个层位的岩石、沉积特征、化石成因及埋藏特征探讨分析后, 证实W. geyiensis化石保存于快速的沉积事件导致的浊流沉积层内, 而化石埋藏的完美程度受到成岩过程中埋藏位置、沉积物中矿物结晶和充填方式的影响, 这些后期的成岩、成矿作用对先期形成的化石精细结构产生了直接和间接的破坏作用。本文通过对W. geyiensis化石体上黏土矿物、草莓状黄铁矿、自形–半自形黄铁矿的成因分析后, 获得最适合保存软躯体化石的环境应该为缺氧且生物体与孔隙水中的硫酸盐无接触的原地和近原地埋藏条件。     

A kinase anchor protein 150 (AKAP150)-associated protein kinase A limits dendritic spine density

The A kinase anchor protein AKAP150 recruits the cAMP-dependent protein kinase (PKA) to dendritic spines. Here we show that in AKAP150 (AKAP5) knock-out (KO) mice frequency of miniature excitatory post-synaptic currents (mEPSC) and inhibitory post-synaptic currents (mIPSC) are elevated at 2 weeks and, more modestly, 4 weeks of age in the hippocampal CA1 area versus litter mate WT mice. Linear spine density and ratio of AMPAR to NMDAR EPSC amplitudes were also increased. Amplitude and decay time of mEPSCs, decay time of mIPSCs, and spine size were unaltered. Mice in which the PKA anchoring C-terminal 36 residues of AKAP150 are deleted (D36) showed similar changes. Furthermore, whereas acute stimulation of PKA (2-4 h) increases spine density, prolonged PKA stimulation (48 h) reduces spine density in apical dendrites of CA1 pyramidal neurons in organotypic slice cultures. The data from the AKAP150 mutant mice show that AKAP150-anchored PKA chronically limits the number of spines with functional AMPARs at 2-4 weeks of age. However, synaptic transmission and spine density was normal at 8 weeks in KO and D36 mice. Thus AKAP150-independent mechanisms correct the aberrantly high number of active spines in juvenile AKAP150 KO and D36 mice during development.     

The crystal structure and mechanism of an unusual oxidoreductase, GilR, involved in gilvocarcin V biosynthesis

GilR is a recently identified oxidoreductase that catalyzes the terminal step of gilvocarcin V biosynthesis and is a unique enzyme that establishes the lactone core of the polyketide-derived gilvocarcin chromophore. Gilvocarcin-type compounds form a small distinct family of anticancer agents that are involved in both photo-activated DNA-alkylation and histone H3 cross-linking. High resolution crystal structures of apoGilR and GilR in complex with its substrate pregilvocarcin V reveals that GilR belongs to the small group of a relatively new type of the vanillyl-alcohol oxidase flavoprotein family characterized by bicovalently tethered cofactors. GilR was found as a dimer, with the bicovalently attached FAD cofactor mediated through His-65 and Cys-125. Subsequent mutagenesis and functional assays indicate that Tyr-445 may be involved in reaction catalysis and in mediating the covalent attachment of FAD, whereas Tyr-448 serves as an essential residue initiating the catalysis by swinging away from the active site to accommodate binding of the 6R-configured substrate and consequently abstracting the proton of the hydroxyl residue of the substrate hemiacetal 6-OH group. These studies lay the groundwork for future enzyme engineering to broaden the substrate specificity of this bottleneck enzyme of the gilvocarcin biosynthetic pathway for the development of novel anti-cancer therapeutics.     

Involvement of autophagy in oncogenic K-Ras-induced malignant cell transformation

Autophagy has recently been implicated in both the prevention and progression of cancer. However, the molecular basis for the relationship between autophagy induction and the initial acquisition of malignancy is currently unknown. Here, we provide the first evidence that autophagy is essential for oncogenic K-Ras (K-Ras(V12))-induced malignant cell transformation. Retroviral expression of K-Ras(V12) induced autophagic vacuole formation and malignant transformation in human breast epithelial cells. Interestingly, pharmacological inhibition of autophagy completely blocked K-Ras(V12)-induced, anchorage-independent cell growth on soft agar. Both mRNA and protein levels of ATG5 and ATG7 (autophagy-specific genes 5 and 7, respectively) were increased in cells overexpressing K-Ras(V12). Targeted suppression of ATG5 or ATG7 expression by short hairpin (sh) RNA inhibited cell growth on soft agar and tumor formation in nude mice. Moreover, inhibition of reactive oxygen species (ROS) with antioxidants clearly attenuated K-Ras(V12)-induced ATG5 and ATG7 induction, autophagy, and malignant cell transformation. MAPK pathway components were activated in cells overexpressing K-Ras(V12), and inhibition of JNK blunted induction of ATG5 and ATG7 and subsequent autophagy. In addition, pretreatment with antioxidants completely inhibited K-Ras(V12)-induced JNK activation. Our results provide novel evidence that autophagy is critically involved in malignant transformation by oncogenic K-Ras and show that reactive oxygen species-mediated JNK activation plays a causal role in autophagy induction through up-regulation of ATG5 and ATG7.