若干有争议的直立人头骨特征在周口店和东非人科成员中的出现情况(英文)

多年来,直立人被看作是一个公认的物种;它曾分布于亚洲和非洲,也可能还曾分布于欧洲。这个物种包括了从距今180万年至距今大约20万年的人科成员。直立人标本彼此之间有着许许多多的相似之处,因此,归属于同一个物种已为众所认可(Howells 1980,Rightmire 1984)。 然而,这一观点好几年来受到一些研究者的质疑(Andrews 1984,Stringer 1984,Wood 1984)。这些研究者使用的是分支系统学方法。使用这种方法是试图复原出演化谱系中分裂出新种和其它分类单元的过程。该方法并不涉及全部相似之点,而是着重于单一的形态性状状态及其变化和分裂情况。依据这一方法,共有的衍生特征或独有的衍生特征对复原物种之间的关系才是有用的。亚洲的与非洲的直立人之间的许多共有性状常只被当作在其它分类单元里也存在的原始性状而已。 根据分支系统学方法,一些研究者(Stringer 1984,Wood 1984)强调:若干0独有的衍生性状状态或特化性仅存在于东亚的直立人之中。Andrews(1984)对原始特征作了进一步地剔除,表列出东亚直立人具有的7个近裔自性:额矢状嵴、顶矢状嵴、厚的颅盖骨、顶骨的角圆枕、枕外隆突点远离枕内隆突点、乳突裂、以及盂内突与鼓板之间的隐窝。 Andrews(1984)根据这些特征提出了一个假说,认为“人类的演化绕过了亚洲     

Characterization of a polymorphism in the 3′ part of the chicken vitellogenin gene

Summary An allele giving rise to a polymorphism within the 3 part of the chicken vitellogenin gene was cloned, sequenced, and compared to the previously cloned allele. The polymorphism is formed by a perfect copy of 343 bp from intron 32 in tandem array with a perfect copy of 244 bp from intron 33; this 587-bp element is inserted in a head-to-tail arrangement in intron 33. We propose a mechanism in which an unequal crossing-over resulted in a vitellogenin gene with two exons 33, one of which was subsequently deleted. Thus, intron 33 was enlarged by the tandem repeats without affecting the protein-encoding sequence of the gene. At the boundaries of the repeated elements, two short direct repeats are found that resemble the recombination signals of immunoglobulin genes. They may have had a key role in the formation of the new allele.     

The high-resolution NMR structure of the R21A Spc-SH3:P41 complex: Understanding the determinants of binding affinity by comparison with Abl-SH3

Background  

SH3 domains are small protein modules of 60–85 amino acids that bind to short proline-rich sequences with moderate-to-low affinity and specificity. Interactions with SH3 domains play a crucial role in regulation of many cellular processes (some are related to cancer and AIDS) and have thus been interesting targets in drug design. The decapeptide APSYSPPPPP (p41) binds with relatively high affinity to the SH3 domain of the Abl tyrosine kinase (Abl-SH3), while it has a 100 times lower affinity for the α-spectrin SH3 domain (Spc-SH3).     

Which stage of the process of apotransketolase interaction with thiamine diphosphate is affected by the regulatory activity of the donor substrate?

The interaction of thiamine diphosphate (ThDP) with transketolase (TK) involves at least two stages: [formula: see text] During the first stage, an inactive intermediate complex (TK...ThDP) is formed, which is then transformed into a catalytically active holoenzyme (TK* - ThDP). The second stage is related to conformational changes of the protein. In the preceding publication (Esakova, O. A., Meshalkina, L. E., Golbik, R., Hübner, G., and Kochetov, G. A. Eur. J. Biochem. 2004, 271, 4189 - 4194) we reported that the affinity of ThDP for TK considerably increases in the presence of the donor substrate, which may be a mechanism whereby the activity of the enzyme is regulated under the conditions of the coenzyme deficiency. Here, we demonstrate that the substrate affects the stage of the reverse conformational transition, characterized by the constant k(-1): in the presence of the substrate, its value is decreased several fold, whereas K(d) and k(+1) remain unchanged.     

Does universal temperature dependence apply to communities? An experimental test using natural marine plankton assemblages

The metabolic theory of ecology (MTE) is an intriguing but controversial theory that tries to explain ecological patterns at all scales on the basis of first principles. Temperature plays a pivotal role in this theory. According to MTE, the Arrhenius relationship that describes the effect of temperature on biochemical reactions extends to a 'universal temperature dependence' that encompasses all kinds of processes and scales up to the cellular, the organismal, and the community level. In this study we test the prediction that community growth rate is temperature dependent in an Arrhenius-like way. First, we performed a literature review of the scanty data on the temperature dependence of the rates of metabolism, photosynthesis and growth of communities. In contrast to the predictions of MTE, the community activation energies did not cluster around 0.32 eV, the activation energy of photosynthesis and primary production or around 0.65 eV, the activation energy of metabolism. However, in none of the published studies the conditions were sufficiently controlled to allow firm conclusions. We therefore also performed replicated and controlled experiments using natural assemblages of marine plankton. As predicted by MTE, the maximal growth rates of community biomass increased linearly in an Arrhenius plot, with a slope close to 0.32 eV. However, a diversity of other models for the temperature dependence of community growth rates fit our data equally well. Hence, our results are at best a weak confirmation of MTE.     

Slow Growth Induces Heat-Shock Resistance in Normal and Respiratory-deficient Yeast

Yeast cells respond to a variety of environmental stresses, including heat shock and growth limitation. There is considerable overlap in these responses both from the point of view of gene expression patterns and cross-protection for survival. We performed experiments in which cells growing at different steady-state growth rates in chemostats were subjected to a short heat pulse. Gene expression patterns allowed us to partition genes whose expression responds to heat shock into subsets of genes that also respond to slow growth rate and those that do not. We found also that the degree of induction and repression of genes that respond to stress is generally weaker in respiratory deficient mutants, suggesting a role for increased respiratory activity in the apparent stress response to slow growth. Consistent with our gene expression results in wild-type cells, we found that cells growing more slowly are cross-protected for heat shock, i.e., better able to survive a lethal heat challenge. Surprisingly, however, we found no difference in cross-protection between respiratory-deficient and wild-type cells, suggesting induction of heat resistance at low growth rates is independent of respiratory activity, even though many of the changes in gene expression are not.