Impact of the Economic Structure of Cities on Urban Scaling Factors: Implications for Urban Material and Energy Flows in China

We explore the population‐scaling and gross domestic product (GDP)‐scaling relationships of material and energy flow (MEF) parameters in different city types based on economic structure. Using migration‐corrected population data, we classify 233 Chinese city propers (Shiqu) as “highly industrial” (share of secondary GDP exceeds 63.9%), “highly commercial” (share of tertiary GDP exceeds 52.6%), and “mixed‐economy” (the remaining cities). We find that, first, the GDP population‐scaling factors differ in the different city types. Highly commercial and mixed‐economy cities exhibit superlinear GDP population‐scaling factors greater than 1, whereas highly industrial cities are sublinear. Second, GDP scaling better correlates with city‐wide MEF parameters in Chinese cities; these scaling relationships also show differences by city typology. Third, highly commercial cities are significantly different from others in demonstrating greater average per capita household income creation relative to per capita GDP. Further, highly industrial cities show an apparent cap in population. This also translates to lower densities in highly industrial cities compared to other types, showing a size effect on urban population density. Finally, a multiple variable regression of total household electricity showed significant and positive correlation with population, income effect, and urban form effect. With such multivariate modeling, the apparent superlinearity of household electricity use with respect to population is no longer observed. Our study enhances understanding of MEFs associated with Chinese cities and provides new insights into the patterns of scaling observed in different city types by economic structure. Results recommend dual scaling by GDP and by population for MEF parameters and suggest caution in applying universal scaling factors to all cities in a country.     

Staufen- and FMRP-containing neuronal RNPs are structurally and functionally related to somatic P bodies

Local control of mRNA translation modulates neuronal development, synaptic plasticity, and memory formation. A poorly understood aspect of this control is the role and composition of ribonucleoprotein (RNP) particles that mediate transport and translation of neuronal RNAs. Here, we show that staufen- and FMRP-containing RNPs in Drosophila neurons contain proteins also present in somatic "P bodies," including the RNA-degradative enzymes Dcp1p and Xrn1p/Pacman and crucial components of miRNA (argonaute), NMD (Upf1p), and general translational repression (Dhh1p/Me31B) pathways. Drosophila Me31B is shown to participate (1) with an FMRP-associated, P body protein (Scd6p/trailer hitch) in FMRP-driven, argonaute-dependent translational repression in developing eye imaginal discs; (2) in dendritic elaboration of larval sensory neurons; and (3) in bantam miRNA-mediated translational repression in wing imaginal discs. These results argue for a conserved mechanism of translational control critical to neuronal function and open up new experimental avenues for understanding the regulation of mRNA function within neurons.     

Sphingobium chlorophenolicum dichlorohydroquinone dioxygenase (PcpA) is alkaline resistant and thermally stable

Dichlorohydroquinone dioxygenase (PcpA) is the ring-cleavage enzyme in the PCP biodegradation pathway in Sphingobium chlorophenolicum strain ATCC 39723. PcpA dehalogenates and oxidizes 2,6-dichlorohydroquinone to form 2-chloromaleylacetate, which is subsequently converted to succinyl coenzyme A and acetyl coenzyme A via 3-oxoadipate. Previous studies have shown that PcpA is highly substrate-specific and only uses 2,6-dichlorohydroquinone as its substrate. In the current study, we overexpressed and purified recombinant PcpA and showed that PcpA was highly alkaline resistant and thermally stable. PcpA exhibited two activity peaks at pH 7.0 and 10.0, respectively. The apparent k(cat) and K(m) were measured as 0.19 ± 0.01 s(-1) and 0.24 ± 0.08 mM, respectively at pH 7.0, and 0.17 ± 0.01 s(-1) and 0.77 ± 0.29 mM, respectively at pH 10.0. Electron paramagnetic resonance studies showed rapid oxidation of Fe(II) to Fe(III) in PcpA and the formation of a stable radical intermediate during the enzyme catalysis. The stable radical was predicted to be an epoxide type dichloro radical with the unpaired electron density localized on C3.     

Genetic Modifiers of dFMR1 Encode RNA Granule Components in Drosophila

Mechanisms of neuronal mRNA localization and translation are of considerable biological interest. Spatially regulated mRNA translation contributes to cell-fate decisions and axon guidance during development, as well as to long-term synaptic plasticity in adulthood. The Fragile-X Mental Retardation protein (FMRP/dFMR1) is one of the best-studied neuronal translational control molecules and here we describe the identification and early characterization of proteins likely to function in the dFMR1 pathway. Induction of the dFMR1 in sevenless-expressing cells of the Drosophila eye causes a disorganized (rough) eye through a mechanism that requires residues necessary for dFMR1/FMRP''s translational repressor function. Several mutations in dco, orb2, pAbp, rm62, and smD3 genes dominantly suppress the sev-dfmr1 rough-eye phenotype, suggesting that they are required for dFMR1-mediated processes. The encoded proteins localize to dFMR1-containing neuronal mRNPs in neurites of cultured neurons, and/or have an effect on dendritic branching predicted for bona fide neuronal translational repressors. Genetic mosaic analyses indicate that dco, orb2, rm62, smD3, and dfmr1 are dispensable for translational repression of hid, a microRNA target gene, known to be repressed in wing discs by the bantam miRNA. Thus, the encoded proteins may function as miRNA- and/or mRNA-specific translational regulators in vivo.THE subcellular localization and regulated translation of stored mRNAs contributes to cellular asymmetry and subcellular specialization (Lecuyer et al. 2007; Martin and Ephrussi 2009). In mature neurons, local protein synthesis at active synapses may contribute to synapse-specific plasticity that underlies persistent forms of memory (Casadio et al. 1999; Ashraf et al. 2006; Sutton and Schuman 2006; Richter and Klann 2009). During this process, synaptic activity causes local translation of mRNAs normally stored in translationally repressed synaptic mRNPs (Sutton and Schuman 2006; Richter and Klann 2009). While specific neuronal translational repressors and microRNAs have been implicated in this process, their involvement in local translation that underlies memory, as well as the underlying mechanisms, are generally not well understood (Schratt et al. 2006; Keleman et al. 2007; Kwak et al. 2008; Li et al. 2008; Richter and Klann 2009). Furthermore, it remains possible that there are neuron-specific, mRNA-specific, and stimulus-pattern specific pathways for neuronal translational control (Raab-Graham et al. 2006; Giorgi et al. 2007).The Fragile-X Mental Retardation protein (FMRP) is among the best studied of neuronal translational repressors, in part due to its association with human neurodevelopmental disease (Pieretti et al. 1991; Mazroui et al. 2002; Gao 2008). Consistent with function in synaptic translation required for memory formation, mutations in FMRP are associated with increased synaptic translation, enhanced LTD, increased synapse growth, and also with enhanced long-term memory (Zhang et al. 2001; Huber et al. 2002; Bolduc et al. 2008; Dictenberg et al. 2008).FMRP co-immunoprecipitates with components of the RNAi and miRNA machinery and appears to be required for aspects of miRNA function in neurons (Caudy et al. 2002; Ishizuka et al. 2002; Jin et al. 2004b; Gao 2008). In addition, FMRP associates with neuronal polyribosomes as well as with Staufen-containing ribonucleoprotein (mRNP) granules easily observed in neurites of cultured neurons (Feng et al. 1997; Krichevsky and Kosik 2001; Mazroui et al. 2002; Kanai et al. 2004; Barbee et al. 2006; Bramham and Wells 2007; Bassell and Warren 2008; Dictenberg et al. 2008). FMRP-containing neuronal mRNPs contain not only several ubiquitous translational control molecules, but also CaMKII and Arc mRNAs, whose translation is locally controlled at synapses (Rook et al. 2000; Krichevsky and Kosik 2001; Kanai et al. 2004; Barbee et al. 2006). Thus, FMRP-containing RNA particles are probably translationally repressed and transported along microtubules from the neuronal cell body to synaptic sites in dendrites where local synaptic activity can induce their translation (Kiebler and Bassell 2006; Dictenberg et al. 2008).The functions of FMRP/dFMR1 in mRNA localization as well as miRNA-dependent and independent forms of translational control is likely to require several other regulatory proteins. To identify such proteins, we used a previously designed and validated genetic screen (Wan et al. 2000; Jin et al. 2004a; Zarnescu et al. 2005). The overexpression of dFMR1 in the fly eye causes a “rough-eye” phenotype through a mechanism that requires (a) key residues in dFMR1 that mediate translational repression in vitro; (b) Ago1, a known components of the miRNA pathway; and (c) a DEAD-box helicase called Me31B, which is a highly conserved protein from yeast (Dhh1p) to humans (Rck54/DDX6) functioning in translational repression and present on neuritic mRNPs (Wan et al. 2000; Laggerbauer et al. 2001; Jin et al. 2004a; Coller and Parker 2005; Barbee et al. 2006; Chu and Rana 2006). To identify other Me31B-like translational repressors and neuronal granule components, we screened mutations in 43 candidate proteins for their ability to modify dFMR1 induced rough-eye phenotype. We describe the results of this genetic screen and follow up experiments to address the potential cellular functions of five genes identified as suppressors of sev-dfmr1.     

Effect of sex steroids on the male reproductive organs of the monitor lizard Varanus monitor (Linn.).

Exogenous sex steroids were administered to adult males of the monitor lizard Varanus during the retrogressive and inactive phases of their annual reproductive cycle. Androgen treatment renews spermatogenetic activity and causes an increase in the number of Leydig cells of the testis during the retrogressive phase; during the inactive phase the testicular response to androgen is only slight. In either reproductive phase oestradiol treatment has an inhibitory action on the germ tubules. Progesterone has no effect on the testis in the inactive phase. The vasa deferentia are well developed during the retrogressive phase and thus the effect of androgens is not appreciable. However, during the inactive phase testosterone highly stimulates the deferent ducts. In the inactive phase oestrogen and progesterone also seem to stimulate slightly the deferent tubules; progesterone increases the interstitial tissue of the deferent ducts. Renal sexual segments hypertrophy and become secretory by androgen treatment in either phase of the reproductive cycle, whereas oestrogen and progesterone have no effect. The hemipenes are also stimulated by androgen treatment.     

The ups and downs of daily life: profiling circadian gene expression in Drosophila

Circadian rhythms are responsible for 24-hour oscillations in diverse biological processes. While the central genes governing circadian pacemaker rhythmicity have largely been identified, clock-controlled output molecules responsible for regulating rhythmic behaviors remain largely unknown. Two recent reports from McDonald and Rosbash(1) and Claridge-Chang et al.2 address this issue. By identifying a large number of genes whose mRNA levels show circadian oscillations, the reports provide important new information on the biology of circadian rhythm. In addition, the reports illustrate both the power and limitations of microarray-based methods for profiling mRNA expression on a genomic scale.     

Spinsters,synaptic defects,and amaurotic idiocy

In this issue of Neuron, Sweeney and Davis present a beautiful characterization of Drosophila mutants in a gene named spinster. The results indicate a function of the endocytic pathway in regulating transforming growth factor-beta (TGF-beta) signaling at the Drosophila motor synapse. This study provides important new information at an intersection of several disciplines, including membrane traffic, lipid organization, synaptic signaling, and neurodegenerative lysosomal storage disease.