Plant responses to elevated CO<Subscript>2</Subscript> concentration at different scales: leaf,whole plant,canopy, and population

Elevated CO₂ enhances photosynthesis and growth of plants, but the enhancement is strongly influenced by the availability of nitrogen. In this article, we summarise our studies on plant responses to elevated CO₂. The photosynthetic capacity of leaves depends not only on leaf nitrogen content but also on nitrogen partitioning within a leaf. In Polygonum cuspidatum, nitrogen partitioning among the photosynthetic components was not influenced by elevated CO₂ but changed between seasons. Since the alteration in nitrogen partitioning resulted in different CO₂-dependence of photosynthetic rates, enhancement of photosynthesis by elevated CO₂ was greater in autumn than in summer. Leaf mass per unit area (LMA) increases in plants grown at elevated CO₂. This increase was considered to have resulted from the accumulation of carbohydrates not used for plant growth. With a sensitive analysis of a growth model, however, we suggested that the increase in LMA is advantageous for growth at elevated CO₂ by compensating for the reduction in leaf nitrogen concentration per unit mass. Enhancement of reproductive yield by elevated CO₂ is often smaller than that expected from vegetative growth. In Xanthium canadense, elevated CO₂ did not increase seed production, though the vegetative growth increased by 53%. As nitrogen concentration of seeds remained constant at different CO₂ levels, we suggest that the availability of nitrogen limited seed production at elevated CO₂ levels. We found that leaf area development of plant canopy was strongly constrained by the availability of nitrogen rather than by CO₂. In a rice field cultivated at free-air CO₂ enrichment, the leaf area index (LAI) increased with an increase in nitrogen availability but did not change with CO₂ elevation. We determined optimal LAI to maximise canopy photosynthesis and demonstrated that enhancement of canopy photosynthesis by elevated CO₂ was larger at high than at low nitrogen availability. We also studied competitive asymmetry among individuals in an even-aged, monospecific stand at elevated CO₂. Light acquisition (acquired light per unit aboveground mass) and utilisation (photosynthesis per unit acquired light) were calculated for each individual in the stand. Elevated CO₂ enhanced photosynthesis and growth of tall dominants, which reduced the light availability for shorter subordinates and consequently increased size inequality in the stand.     

SER-7, a Caenorhabditis elegans 5-HT7-like receptor, is essential for the 5-HT stimulation of pharyngeal pumping and egg laying

Serotonin (5-HT) stimulates both pharyngeal pumping and egg laying in Caenorhabditis elegans. Four distinct 5-HT receptors have been partially characterized, but little is known about their function in vivo. SER-7 exhibits most sequence identity to the mammalian 5-HT7 receptors and couples to a stimulation of adenyl cyclase when expressed in COS-7 cells. However, many 5-HT7-specific agonists have low affinity for SER-7. 5-HT fails to stimulate pharyngeal pumping and the firing of the MC motorneurons in animals containing the putative ser-7(tm1325) and ser-7(tm1728) null alleles. In addition, although pumping on bacteria is upregulated in ser-7(tm1325) animals, pumping is more irregular. A similar failure to maintain "fast pumping" on bacteria also was observed in ser-1(ok345) and tph-1(mg280) animals that contain putative null alleles of a 5-HT2-like receptor and tryptophan hydroxylase, respectively, suggesting that serotonergic signaling, although not essential for the upregulation of pumping on bacteria, "fine tunes" the process. 5-HT also fails to stimulate egg laying in ser-7(tm1325), ser-1(ok345), and ser-7(tm1325) ser-1(ok345) animals, but only the ser-7 ser-1 double mutants exhibit an Egl phenotype. All of the SER-7 mutant phenotypes are rescued by the expression of full-length ser-7gfp translational fusions. ser-7gfp is expressed in several pharyngeal neurons, including the MC, M2, M3, M4, and M5, and in vulval muscle. Interestingly, 5-HT inhibits egg laying and pharyngeal pumping in ser-7 null mutants and the 5-HT inhibition of egg laying, but not pumping, is abolished in ser-7(tm1325);ser-4(ok512) double mutants. Taken together, these results suggest that SER-7 is essential for the 5-HT stimulation of both egg laying and pharyngeal pumping, but that other signaling pathways can probably fulfill similar roles in vivo.     

激光及γ射线对有丝分裂染色体畸变感应现象的比较

波长514nm的激光照射可用于研究激光导致有丝分裂染色体畸变的效应。本文提供了一种新的辐照系统,能用于研究突变的感应现象,并与从γ-线辐射源获得的结果进行了比较。 Abstract:Laser irradiation at wavelength 514 nm was used to study the effect of lasers in inducing chromosomal aberrations at mitosis.This study offers a new radiation system which could be used for the induction of mutations.Results are compared with those obtained from studies using γ-rays as irradiation source.     

禽流感H5N1病毒感染BALB/c小鼠后多器官病变初探

为了研究禽流感H5N1病毒在各个器官的增殖和病理变化,在生物安全实验室,我们将禽流感H5N1病毒通过尾静脉接种BALB/C小鼠。结果小鼠在不经过适应的情况下,直接感染发病,甚至死亡。在观察的7天内,感染小鼠临床症状主要表现呼吸急促,体温、体重下降。尸检表现肺出血,心外膜坏死以及肝脏的坏死。组织病理检查表现心、肝、肺等多器官的病变。肺的病变伴有纤维化的弥漫性肺泡损伤;心肌外膜大量淋巴细胞浸润、坏死;肝细胞大量坏死,淋巴细胞浸润。心、肝的坏死病变在H5N1禽流感病毒相关的研究中未见报道。经过对各个组织器官的病毒载量的检测,未发现病毒在各个病变组织中的复制。免疫组化的检测,各个组织中也未检出阳性的细胞反应。因此,我们认为H5N1禽流感病毒感染小鼠引起多个器官组织的损伤,甚至死亡,不是病毒在器官的复制,而可能是病毒感染小鼠,产生炎症细胞因子的高度表达,损伤多个器官组织所致。     

Phosphorylation and inactivation of the pyruvate dehydrogenase from the anaerobic parasitic nematode, Ascaris suum. Stoichiometry and amino acid sequence around the phosphorylation sites

Tryptic digestion of the fully phosphorylated Ascaris suum pyruvate dehydrogenase complex yielded a single tetradecapeptide containing 2 phosphorylated serine residues. Its amino acid sequence was Tyr-Ser-Gly-His-Ser(P)-Met-Ser-Asp-Pro-Gly-Thr-Ser(P)-Tyr-Arg and was very similar to one of the tryptic phosphopeptides isolated from mammalian and yeast pyruvate dehydrogenases. At partial phosphorylation, three peptides were isolated which corresponded to the monophosphorylated (sites 1 and 2) and diphosphorylated tetradecapeptides. In contrast to results reported from mammalian complexes, phosphorylation of the ascarid complex paralleled inactivation, and no additional phosphorylation occurred after inactivation was complete. Complete inactivation of the complex was associated with the incorporation of 1.7-1.9 mol of phosphoryl groups/mol of alpha-pyruvate dehydrogenase subunit, and the strict preference of the pyruvate dehydrogenase kinase for site 1 was not observed. Whereas site 1 was initially phosphorylated more rapidly than site 2, at 50% inactivation, 41% of the incorporated phosphoryl groups were incorporated into site 2. In addition, substantial amounts of peptide monophosphorylated at site 2 also accumulated, suggesting that prior phosphorylation at site 1 was not necessary for phosphorylation at site 2. Phosphorylation also caused a marked decrease in the mobility of the alpha-pyruvate dehydrogenase subunit on sodium dodecyl sulfate-polyacrylamide gels and the apparent separation of mono- and diphosphorylated forms of the enzyme. The significance of these observations in the regulation of the unique anaerobic mitochondrial metabolism of A. suum is discussed.     

A Genetic Survey of Fluoxetine Action on Synaptic Transmission in Caenorhabditis elegans

Fluoxetine is one of the most commonly prescribed medications for many behavioral and neurological disorders. Fluoxetine acts primarily as an inhibitor of the serotonin reuptake transporter (SERT) to block the removal of serotonin from the synaptic cleft, thereby enhancing serotonin signals. While the effects of fluoxetine on behavior are firmly established, debate is ongoing whether inhibition of serotonin reuptake is a sufficient explanation for its therapeutic action. Here, we provide evidence of two additional aspects of fluoxetine action through genetic analyses in Caenorhabditis elegans. We show that fluoxetine treatment and null mutation in the sole SERT gene mod-5 eliminate serotonin in specific neurons. These neurons do not synthesize serotonin but import extracellular serotonin via MOD-5/SERT. Furthermore, we show that fluoxetine acts independently of MOD-5/SERT to regulate discrete properties of acetylcholine (Ach), gamma-aminobutyric acid (GABA), and glutamate neurotransmission in the locomotory circuit. We identified that two G-protein–coupled 5-HT receptors, SER-7 and SER-5, antagonistically regulate the effects of fluoxetine and that fluoxetine binds to SER-7. Epistatic analyses suggest that SER-7 and SER-5 act upstream of AMPA receptor GLR-1 signaling. Our work provides genetic evidence that fluoxetine may influence neuronal functions and behavior by directly targeting serotonin receptors.FLUOXETINE is a selective serotonin reuptake inhibitor (SSRI) and has made a major impact on the treatment of many behavioral disorders. The empirical action of SSRIs is blocking the serotonin reuptake transporter (SERT). SERT is localized in the plasma membrane and transports extracellular serotonin (5-HT) into the cytoplasm (Blakely et al. 1991; Hoffman et al. 1991), this being the major mechanism of terminating 5-HT signaling. Consequently, SSRIs are thought to exert therapeutic effects by blocking SERT from removal of 5-HT in the synaptic clef, thereby increasing the level of 5-HT signals (Schatzberg and Nemeroff 2004). However, several observations point to additional actions of SSRIs on the 5-HT system and neuronal functions. First, knockout of SERT in mouse caused a marked reduction of 5-HT in the brain (Bengel et al. 1998). Second, a variety of studies with cultured mammalian cells and mouse brain slices showed that SSRIs and tricyclic antidepressant agents (TCAs) have high affinities to many 5-HT receptor subtypes and act as agonists or antagonists depending on particular receptors being tested (Ni and Miledi 1997; Kroeze and Roth 1998; Eisensamer et al. 2003). Third, genetic analyses of the nematode Caenorhabditis elegans in our laboratory and others showed that fluoxetine and the TCA imipramine (Tofrani) could influence behavior independent of SERT function (Weinshenker et al. 1995; Ranganathan et al. 2001; Dempsey et al. 2005). In this study, we carried out a systematic survey of SSRIs treatment in C. elegans to gain new insights into actions of SSRIs on the 5-HT system and other neurotransmitter systems.In both vertebrates and invertebrates, 5-HT functions as a neuromodulator to either facilitate or inhibit synaptic transmission of other neurotransmitters (Fink and Gothert 2007). Modulation of synaptic activity by 5-HT signaling underscores the synaptic plasticity involved in stress responses, learning, adaptation, and memory (Kandel 2001; Zhang et al. 2005). The role of 5-HT in C. elegans was initially identified through pharmacological experiments showing that exogenous 5-HT can promptly induce changes in a variety of behaviors, including feeding, egg laying, and locomotion (Avery and Horvitz 1990; Weinshenker et al. 1995; Nurrish et al. 1999). The relevance of these behaviors to endogenous 5-HT has since been validated through studies of mutants of 5-HT signaling. Importantly, multiple 5-HT receptors may function in distinct cells synergistically or antagonistically to regulate a specific behavior (Carnell et al. 2005; Dernovici et al. 2007; Murakami and Murakami 2007; Hapiak et al. 2009). In nearly all tested paradigms, fluoxetine and imipramine induce behavioral changes similarly to exogenous 5-HT (Weinshenker et al. 1995; Nurrish et al. 1999), implying that fluoxetine regulates 5-HT inputs to these neural circuits. However, the tryptophan hydroxylase gene tph-1 is required for 5-HT biosynthesis in C. elegans (Sze et al. 2000), mod-5 encodes its sole SERT (Ranganathan et al. 2001), and yet fluoxetine could stimulate egg laying and inhibit locomotion in mod-5 and tph-1 mutants (Weinshenker et al. 1995; Choy and Thomas 1999; Ranganathan et al. 2001; Dempsey et al. 2005). These findings provided a basis for further investigation into genes and synaptic functions regulated by 5-HT and the impact of fluoxetine on 5-HT signaling.Here we present genetic evidence of multifaceted effects of fluoxetine on the 5-HT system and its downstream targets in C. elegans. We show that fluoxetine treatment and loss of MOD-5/SERT function do not simply increase presynaptic 5-HT signals. Rather, they may eliminate 5-HT in specific neurons. Furthermore, fluoxetine acts independently of SERT to regulate 5-HT serotonin receptors and their downstream targets involved in acetylcholine (ACh), gamma-aminobutyric acid (GABA), and glutamate neurotransmission.