Working toward solutions requires transdisciplinary and integrative approaches to systematic understanding, goal setting, strategy development, and implementation (Jerneck et al. 2011).

The papers in this Special Issue provide some of the pieces to build the capacity to answer and act on these questions in small island communities around the world. References Adger WN (2006) Vulnerability. Global Environ Change 16:268–281CrossRef Adger WN, Hughes TP, Folke C, Carpenter SR, Rockström J (2005) Social-ecological resilience to coastal disasters. Science 309:1036–1039CrossRef Forbes DL, James TS, Sutherland M, Nichols SE (2013) Physical basis of coastal adaptation on tropical small islands. Sustain Sci (this volume). doi: 10.​1007/​s11625-013-0218-4 Hay JE (2013) Small island developing buy Eltanexor states: coastal systems, global change and sustainability. Sustain Sci (this volume). doi:10.​1007/​s11625-013-0214-8 IPCC (2007) Summary for policymakers. In: Parry ML, Canziani

OF, Palutikof JP, van der Linden PJ, Hanson CE (eds) Climate change 2007: impacts, adaptation and vulnerability. Contribution of Working Group II to the Fourth Assessment Report of the Intergovernmental Panel on Climate Change. Cambridge University Press, Cambridge, pp 7–22 Jerneck A, this website Olsson L, Ness B, Anderberg S, Baier M, Clark E, learn more Hickler T, Hornborg A, Kronsell A, Lövbrand E, Persson J (2011) Structuring sustainability science. Sustain Sci 6:69–82CrossRef Kates R, Clark WC, Correll R, Hall JM, Jaeger CC, Lowe I, McCarthy JJ, Schellnhuber H-J, Bolin B, Dickson NM, Faucheux S, Gallopin GC, Gruebler A, Huntley B, Jager J, Jodha NS, Kasperson RE, Mabogunje A, Matson P, Mooney H, Moore B III, O’Riordan T, Svedin U (2000) Sustainability science.

JF Kennedy School of Government, Harvard University, Cambridge. KSG Working Paper 00-018. http://​ssrn.​com/​abstract=​257359 Mimura N, Nurse L, McLean R, Agard J, Briguglio L, Lefale P, Payet R, Sem G and 7 contributing authors (2007) Small islands. In: Parry Forskolin manufacturer ML, Canziani OF, Palutikof JP, van der Linden PJ, Hanson CE (eds) Climate change 2007: impacts, adaptation and vulnerability. Contribution of Working Group II to the Fourth Assessment Report of the Intergovernmental Panel on Climate Change, Cambridge University Press, Cambridge, pp 687–716 Pelling M, Uitto JI (2001) Small island developing states: natural disaster vulnerability and global change. Environ Hazards 3:49–62CrossRef Turner BL II (2010) Vulnerability and resilience; coalescing or paralleling approaches for sustainability science? Global Environ Change 20:570–576CrossRef”
“Introduction Anthropogenic pollution in reef-flat seawater is of great concern for coastal conservation.

Yan et al. suggested that GBs in CIGS electrically benign and not harmful to photovoltaic due to not creating deep levels [16]. On the other hand, valence band maximum at GBs

acts as hole barriers, it reduces recombination at GBs [17]. Recently, Abou-Ras et al. identified Se-Se-terminated Σ3112 twin boundaries, indicating that Cu is depleted and In is enriched in the two atomic planes next to the twin boundary by high-resolution scanning transmission electron microscopy selleck and electron energy-loss spectroscopy [18]. Takahashi group in Japan also reported that downward band bending of the conduction band and broadening of the band gap near GBs are observed by photo-assisted Kelvin probe force microscopy. It accounts for photo-carriers well separate Ilomastat and suppress the recombination at GBs [19]. Therefore, we have to investigate carefully carrier transport at GB in CZTSSe thin films, which is not yet Talazoparib concentration clearly identified for the role of GBs. We already reported positive potential bending of GBs on CZTSe thin films, grown by electron co-evaporation, which showed 2% to 3% of conversion efficiency [20]. In this study, we investigate sputtered CZTSSe thin-film solar cells, which exhibit better device performance than the previous samples. We report local carrier transport and surface potential of CZTSSe thin films using conductive atomic force microscopy (C-AFM) and Kelvin

probe force microscopy (KPFM), respectively. For the complete understanding of the behaviors at GBs in CIGS films, recombination at GBs is diminished also due O-methylated flavonoid to downward band bending reduced density of deep-level in-gap states (i.e.,

recombination centers) and expect relatively efficient minority-carrier collection at GBs, as shown by scanning tunneling microscopy (STM) measurements [21, 22]. Future analysis using STM can be addressed for GBs of CZTSSe thin films. Method CZTSSe thin films were grown on Mo-coated soda-lime glass substrates. The metal precursor layers were deposited by radio frequency sputtering using Cu, ZnS and SnS targets. The staking order of the precursors in this study was Cu/SnS/ZnS/Mo/glass. Thickness of each stacked layer was changed from 0.4 to 0.7 μm. After the deposition, the precursors were annealed with Se metals in a furnace at 590°C for 20 min. Thickness of the annealed CZTSSe film was 1.8 μm for this study. From X-ray diffraction, the film shows single phase of CZTSSe without any significant second phases. We obtained the final composition is Cu/(Zn + Sn) ~ 0.94 and Zn/Sn ~ 1.65 of CZTSSe thin films by energy dispersive spectrometry (EDS). S/Se ratio is estimated to be approximately 0.1. The grain size indicates 1 to 2 μm of the CZTSSe thin film investigated by field emission scanning electron microscopy (FE-SEM) (JSM-700 F). KPFM and C-AFM measurements were carried out using a commercial AFM (n-Tracer, Nanofocus Inc., Seoul, South Korea).

PubMedCrossRef 11. Crane J, Naeher T, Shulgina I, Zhu C, Boedeker E: Effect of zinc

in enteropathogenic Escherichia coli infection. Infect Immun 2007, 75:5974–5984.PubMedCrossRef DMXAA 12. Cornelis G: The type III secretion injectisome. Nat Rev Microbiol 2006, 4:811–825.PubMedCrossRef 13. Elliott S, Wainwright L, McDaniel T, Jarvis K, Deng Y, Lai L, McNamara B, Donnenberg M, Kaper J: The complete sequence of the locus of enterocyte effacement (LEE) from enteropathogenic Escherichia coli e2348/69. Mol Microbiol 1998, 28:1–4.PubMedCrossRef 14. Mellies J, Elliott S, Sperandio V, Donnenberg M, Kaper J: The Per regulon of enteropathogenic Escherichia coli: identification of a regulatory cascade and a novel transcriptional activator, the locus of enterocyte effacement (LEE)-encoded regulator (Ler). Mol Microbiol 1999, 33:296–306.PubMedCrossRef 15. Crane J, Byrd I, Boedeker E: Virulence inhibition by zinc in shiga-toxigenic MRT67307 order Escherichia coli. Infect Immun 2011, 79:1696–1705.PubMedCrossRef 16. Torres A, López-Sánchez G, Milflores-Flores L, Patel S, Rojas-López M, Martínez de la Peña C, Arenas-Hernández M, Martínez-Laguna Y: Ler and H-NS, regulators controlling expression of the long polar fimbriae of Escherichia coli O157:H7. J

click here Bacteriol 2007, 189:5916–5928.PubMedCrossRef 17. Mellies J, Benison G, McNitt W, Mavor D, Boniface C, Larabee F: Ler of pathogenic Escherichia coli forms toroidal protein-DNA complexes. Microbiology 2011, 157:1123–1133.PubMedCrossRef 18. Outten C, O’Halloran T: Femtomolar sensitivity of metalloregulatory proteins controlling zinc homeostasis. Sci 2001, 292:2488–2492.CrossRef 19. Levine M: Escherichia coli that cause diarrhea: enterotoxigenic, enteropathogenic, enteroinvasive, enterohemorrhagic, and enteroadherent. J Infect Dis 1987, 155:377–389.PubMedCrossRef 20. Jerse A, Yu J, Tall B, Kaper J: A genetic locus of enteropathogenic Escherichia coli necessary

for the Amino acid production of attaching and effacing lesions on tissue culture cells. Proc Natl Acad Sci U S A 1990, 87:7839–7843.PubMedCrossRef 21. Casadaban M: Transposition and fusion of the lac genes to selected promoters in Escherichia coli using bacteriophage lambda and Mu. J Mol Biol 1976, 104:541–555.PubMedCrossRef 22. Patzer S, Hantke K: The zinc-responsive regulator Zur and its control of the znu gene cluster encoding the ZnuABC zinc uptake system in Escherichia coli. J Biol Chem 2000, 275:24321–24332.PubMedCrossRef 23. Pruteanu M, Neher S, Baker T: Ligand-controlled proteolysis of the Escherichia coli transcriptional regulator ZntR. J Bacteriol 2007, 189:3017–3025.PubMedCrossRef 24. Tam C, Missiakas D: Changes in lipopolysaccharide structure induce the sigma(E)-dependent response of Escherichia coli. Mol Microbiol 2005, 55:1403–1412.PubMedCrossRef 25.

5 AB739317 99.4 6 W-Rhino39 1 Methanobrevibacter smithii 97.6 AB739317 99.6 6 W-Rhino41 MLN4924 nmr 2 Methanobrevibacter smithii 97.4 AB739317 99.3 6 W-Rhino42 1 Methanobrevibacter smithii 97.4 AB739317 99.4 6 W-Rhino46 1 Methanobrevibacter smithii 97.5 AB739317 99.4 7 W-Rhino2 3 Methanocorpusculum labreanum 95.4 p38 MAPK cancer AB739382 96.2 7 W-Rhino3 1 Methanocorpusculum labreanum 95.4 AB739382 96.2 7 W-Rhino5 5 Methanocorpusculum labreanum 95.2 AB739382 96.2 7 W-Rhino6 9 Methanocorpusculum labreanum 95.2 AB739382 95.7 7 W-Rhino9 4 Methanocorpusculum labreanum

95.4 AB739382 96.2 7 W-Rhino10 1 Methanocorpusculum labreanum 95.4 AB541926 96.0 7 W-Rhino11 3 Methanocorpusculum labreanum 95.1 AB541926 95.8 7 W-Rhino12 7 Methanocorpusculum labreanum 95.1 AB541926 95.6 7 W-Rhino14 2 Methanocorpusculum labreanum 95.2 AB541926 95.8 7 W-Rhino17 2 Methanocorpusculum labreanum 95.1 AB739382 95.9 7 W-Rhino18 1 Methanocorpusculum labreanum 95.3 AB739382 96.1 7 W-Rhino24 2 Methanocorpusculum labreanum 95.4 AB739382 96.2 7 W-Rhino27 1 Methanocorpusculum labreanum 95.6 AB541926 96.0 7 W-Rhino29 7 Methanocorpusculum labreanum 95.3 AB739382 96.1 7 W-Rhino31 1 Methanocorpusculum labreanum 95.3 AB739382 96.1 7 W-Rhino32 2 Methanocorpusculum labreanum 96.2 AB739400 96.9 7 W-Rhino37 5 Methanocorpusculum labreanum 95.3 AB739382 96.1 7 W-Rhino40 1 Methanocorpusculum labreanum 95.2 AB739382 96.0 7 W-Rhino43 3 Methanocorpusculum labreanum 95.4 AB739382

96.2 7 W-Rhino47 4 Methanocorpusculum labreanum 95.2 AB739382 96.0 Totals   153         *Nearest valid taxon with the same name means the same strain. Figure 2 Rarefaction Selleck GS-1101 curve of the archaeal 16S rRNA clone library obtained from hindgut of the white rhinoceroses. At the phylotype level, W-Rhino1 and W-Rhyno21 (both assigned to OTU-1) were closely related to an uncharacterized archaeal clone from pig feces (99.4% and 99.8% identities, respectively) [14] (Table 1, Figure 1). Reverse transcriptase The two phylotypes belonging to OTU-2 had

98.6% identity to an uncultured clone from bovine rumen [22] (Table 1, Figure 1). Two sequences were related to two methanogen clones (JN030604 and JN030608) from continental shelf of India with 96.0% and 95.7% identity, respectively (Table 1, Figure 1). Five sequences assigned to OTU-7 showed genus-level (95.6% to 96%) sequence identity to an uncharacterized clone from cattle manure [23], while the remaining phylotypes that were assigned to OTU-7 were related to a methanogen clone from the hindgut of the pony (AB739382) with 95.7% to 96.9% identities (Table 1, Figure 1). All phylotypes assigned to OTU-5 also showed genus-level (95.7 to 96.3%) sequence identity to a clone from the hindgut of the pony (AB739382) (Table 1, Figure 1). The clone library OTU coverage rate was 95.4%, indicating that the library was very well sampled for the diversity it contained. Phylogenetic analysis indicated that all 47 phylotypes (i.e., 153 sequences) belonged to four monophyletic groups (Figures 1 and 3).

6 kDa) was sequenced at the Protein Core Facility of the Institute for Cellular and Molecular Biology, University of Texas at Austin. Construction of the XAV-939 plasmid for complementation of the gluQ-rs mutation This plasmid was constructed from the pATGGQRS plasmid in which the T7 promoter was removed by digestion with BglII and NcoI enzymes and replaced by the TRC promoter obtained from pTRC99a plasmid by amplification and digestion with BamHI and NcoI to obtain the pTRCGQ plasmid. The empty plasmid (pCM) was constructed by

incorporating the TRC promoter into the pET15c plasmid. Inactivation of gluQ-rs gene in S. flexneri Deletion of gluQ-rs was carried out using the λ red recombinase method [44] with the following modifications. S. flexneri 2457T carrying pKD46 and prepared as described elsewhere [44] was transformed Kinase Inhibitor Library with a purified PCR fragment amplified from the E. coli ΔgluQ-rs::kan mutant strain using primers dksAF and pcnBR (Table 2), increasing the homologous DNA region to more than 450 bp at each side. The mutant was isolated following overnight growth at 37°C on LB-agar containing kanamycin (50 μg/ml). The deletion was confirmed by PCR using the same pair of primers (dksAF-pcnBR) and using each primer together with an internal primer as described previously [44]. The presence of the S. flexneri virulence plasmid was also confirmed by PCR amplification of the virF gene using primers virFF and virFR (Table 2). Effect of the absence

of gluQ-rs gene in S. flexneri metabolism The effect of the deletion of the gluQ-rs gene on the metabolism of S. flexneri was analyzed by Biolog phenotype MicroArrays following the manufacturer’s instructions click here (Biolog, Inc., Almeda, CA). Strains were grown at 30°C overnight and 5 ml of LB was inoculated with a 1:100 dilution and grown at 37°C to reach an OD650nm of 0.5. The cells were then washed and resuspended to 2.5 x 107 cfu/ml and diluted 200 fold in to a solution of IF-10a medium (Biolog). Each well was inoculated with 1.2 x 104 cfu (0.1 ml per well) into the corresponding plates and incubated for 24

hrs at 37°C. The metabolism was recorded and analyzed by the Omnilog software (V 1.20.02) (Biolog, Inc., Almeda, CA). Acknowledgements We are grateful old to Dr. Dieter Söll from Yale University, USA, for providing the E. coli strains BL21(DE3) and W3110 ΔgluQ-rs::kan. Also, we would like to thank to Dr. Claude Parsot from the Institute Pasteur, France, for providing the pQF50 plasmid and advice in the determination of the N-terminal sequence of GluQ-RS. We appreciate Dr. Elizabeth Wyckoff for her critical review of this manuscript. This publication was funded by Grants from the Department of Research, University of Chile DI I2 06/04-2 and Fondo Nacional de Desarrollo Científico y Tecnólogico (FONDECYT) 1080308 to J.C.S. and Grant AI 169351 from the National Institutes of Health to S.M.P. References 1. Ibba M, Söll D: Aminoacyl-tRNA synthesis. Annu Rev Biochem 2000, 69:617–650.

These results showed that the CNFs produced at 700°C had the highest quantity of graphitic carbon and were similar to those reported in previous studies where Fe-supported catalysts were used [42]. Figure 3 Raman spectra and I D / I G ratios. (a) Laser Raman spectra of as-received coal fly ash and the products from fly ash exposed to acetylene at various temperatures. (b) I D/I G ratios of the CNFs synthesized in acetylene. The D and G band peaks confirmed the formation of CNFs that were identified by TEM. CNFs at 500°C displayed the highest degree of disorder. Figure 4 The first-order weight derivatives of as-received and acetylene-treated

coal fly ash at varying temperatures. CNFs at 700°C displayed the highest oxidation temperature, but CNFs at 500°C displayed Selleck H 89 a bimodal oxidation BV-6 profile. Thermogravimetric studies Thermogravimetric analyses were carried out to investigate the thermal degradation behaviour of as-received and acetylene-treated fly ash. It has been reported that the graphitic nature of CNMs is directly proportional to their

thermal stability [43]. Hence, the first-order weight derivatives of the data so obtained typically gives an indication of the type of carbon present (Figure 4). Typically, highly crystalline nanofibers have been found to be resistant to oxidation when compared to other forms of carbon [44]. Additionally, the diameters and the amount of defects

in such materials have also been known to influence their oxidation buy BI 10773 temperatures [36]. From the TGA thermograms, it was observed that all of the CNMs produced had final oxidation temperatures that were greater than 550°C. However, as previously stated, at least two different forms of carbon were synthesized when the reaction temperature was 500°C. These may have Galactosylceramidase arisen due to the poor carbonization of acetylene, leading to impurities such as amorphous carbon and hence the formation of a higher degree of non-graphitic carbonaceous materials, as confirmed by the laser Raman results (Figure 3a). However, CNFs synthesized at 700°C had the highest oxidation temperature (c.a. 690°C). These results concurred with the laser Raman data, where CNFs formed at 700°C displayed the lowest I D/I G ratio, i.e. they were the most graphitic. Particle size and surface area measurements The particle sizes and surface areas of the as-received and acetylene-treated coal fly ash which reacted at temperatures between 400°C and 700°C are depicted in Figures 5,6,7. As-received coal fly ash, when analysed in water, had a particle size of 160 μm. After exposure to acetylene at 700°C, this size was reduced to 130 μm. A small reduction in the particle size was anticipated, as the fly ash particles were entrained in the CNFs, hence reducing their agglomeration.

65 PG1948 Lipoprotein, putative −1.56 PG0670 Lipoprotein, putative −1.54 PG2155 Lipoprotein, putative −1.53 PG1600 GDC-0068 in vitro Hypothetical Evofosfamide purchase protein −1.52 PG0188 Lipoprotein, putative

1.66 PG0192 Cationic outer membrane protein OmpH 2.68 PG0193 Cationic outer membrane protein OmpH 2.18 PG0717 Lipoprotein, putative 1.95 PG0906 Lipoprotein, putative 1.94 PG1452 Lipoprotein, putative 1.52 PG1828 Lipoprotein, putative 1.87 PG2105 Lipoprotein, putative 1.98 PG2224 Hypothetical protein 2.19 DNA metabolism : DNA replication, recombination, and repair PG1814 DNA primase −2.01 PG1993 Excinuclease ABC, C subunit −1.77 PG1255 Recombination protein RecR −1.64 PG1253 DNA ligase, NAD-dependent −1.62 PG0237 Uracil-DNA glycosylase −1.58 PG1378 A/G-specific adenine glycosylase −2.83 PG1622 DNA topoisomerase IV subunit A −2.02 PG1794 DNA polymerase type I −1.51 PG2009 DNA repair protein RecO, putative 2.34 Purines, pyrimidines, nucleosides, and nucleotides : 2′-Deoxyribonucleotide metabolism PG1129 Ribonucleotide reductase −2.30 PG0953 Deoxyuridine 5′-triphosphate

nucleotidohydrolase −2.14 Purines, pyrimidines, nucleosides, and nucleotides : Nucleotide and nucleoside interconversions PG0512 Guanylate kinase −1.89 Purines, pyrimidines, nucleosides, and nucleotides : Pyrimidine ribonucleotide biosynthesis PG0529 Carbamoyl-phosphate synthase small subunit −1.70 PG0357 Aspartate carbamoyltransferase catalytic subunit −1.54 Purines, pyrimidines, nucleosides, and nucleotides : Salvage of nucleosides and nucleotides PG0558

Purine nucleoside phosphorylase Staurosporine concentration −1.51 PG0792 Hypoxanthine phosphoribosyltransferase 2.25 aLocus number, putative identification, and cellular role are according to the TIGR genome database. bAverage fold difference indicates the expression of the gene by polyP addition versus no polyP addition. cThe cut off ratio for the fold difference was < 1.5. In several transcriptional profiling studies using gram-positive bacteria, a cell wall stress stimulon that includes genes involved Metformin in peptidoglycan biosynthesis was induced in the cells challenged with cell wall-active antibiotics [33,34]. The bacterial cells appeared to respond to the cell wall-active antibiotics by attempting to raise the rate of peptidoglycan biosynthesis in order to compensate for the damaged and partially missing cell wall [35,36]. Overall, the results indicate that the mode of action of polyP against P. gingivalis may be different from not only that of the cell wall-active antibiotics against gram-positive bacteria, but also that of polyP against gram-positive bacteria. Ribosomal proteins In bacteria, production of ribosome requires up to 40% of the cell’s energy in rapidly growing bacteria and is therefore tightly regulated on several levels [37]. It seems that bacteria with kinetically impaired ribosomes can to some extent increase the number of ribosomes accumulated under poor growth conditions or under antibiotic challenge in order to compensate for their slower function [38,39].

We generated a rnhA recG proB::rnhA + strain in which the recG deletion was covered by pJJ100 (pRC7 recG + ). As shown in Figure 3A, only very small

white colonies were observed after incubation for 48 h on LB agar without arabinose. These white colonies are formed due to the leakiness of the araBAD promoter. In contrast, on LB agar with moderate arabinose concentrations robust segregation of blue and white colonies was observed, with the white colonies being as healthy as the blue. Thus, expression of the integrated rnhA construct can be regulated by the presence or Selleckchem AZD5363 absence of arabinose. Figure 3 The lethality of ΔtopA cells is not suppressed by increased levels of RNase HI. (A) Expression Bafilomycin A1 molecular weight of a P araBAD rnhA construct integrated into the chromosome can be regulated by different arabinose concentrations. The expression level is high enough to suppress the synthetic lethality of rnhA recG cells. (B) Expression from the integrated P araBAD rnhA construct does not suppress the lethality of ΔtopA cells. The P araBAD rnhA construct has been integrated into a rnhA + background. Thus, expression of the construct will produce RNase HI in addition to the regular rnhA locus. (C) Expression from the integrated P araBAD rnhA construct does not improve growth of cells in which the ΔtopA

defect is partially suppressed by overexpression of DNA topoisomerase III. The image for AS1066 was reproduced from Figure 2 for comparison. Please note that incubation and image capturing procedures are standardised to allow comparison of colony GSK872 cost sizes To test whether increased Thymidylate synthase levels of RNase HI can suppress the lethality of topA strains

we integrated our proB::rnhA + expression construct into an rnhA + background. Thus, any expression from our integration construct will be in addition to the expression from the native rnhA gene. We then introduced our topA::apra allele, covering the deletion with the pRC7 topA plasmid. However, growth of this strain in medium with moderate (data not shown) or high arabinose concentrations did not lead to formation of white colonies (Figure 3B). Since we did not directly measure the concentration of RNase HI in cells we cannot exclude the possibility that the levels in our expression constructs are not high enough for suppression of the ΔtopA phenotype. We therefore wanted to test the expression of rnhA in a system that might be more sensitive for low expression levels. It was observed before that the co-expression of both rnhA and topB resulted in a synergistic suppression of the topA phenotype [14]. We therefore wanted to know whether the expression of rnhA from our integration construct would increase the suppression of the observed topB overexpression. To test this we transformed our ptopA/ΔtopA ΔproB::rnhA + background with the topB expression plasmid. However, co-expression did not lead to an increase in the size of the white colonies. If anything a mild reduction of viability is observed (Figure 3C).

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This study describes aspects of the natural history of an abundant gall wasp and its most common parasitoids and inquilines. Methods Natural history of gall wasp The cynipid gall-inducer, A. quercuscalifornicus, induces a 5–250 cc (often apple-sized), multilocular (many wasps per gall) gall on the twigs of valley oak (Quercus lobata), a California endemic, where galls become Selleck Compound Library apparent on twigs with bimodal peaks of development which occur in the late spring and mid summer (Rosenthal and Koehler 1971b). It has also been collected from closely-related

oak species, Q. douglasii, Q. berberidifolia, and Q. garryana (Weld 1957). Gall abundances vary widely between individual trees, and extremely high gall densities of more than selleck chemicals 50 galls per cubic meter

of canopy may be supported by some trees. The range of A. quercuscalifornicus spans most of California with the extremes of southern Washington and northern Mexico (Russo 2006). Initially, the developing galls are green and moist throughout, but towards fall the external wall of the gall becomes harder, and the entire gall desiccates (“maturation date” in this study). Larvae grow and differentiate until fall, when fully developed adults emerge. Descriptions exist only for females of A. quercuscalifornicus, and the species is thought to be entirely parthenogenetic and univoltine (Schick 2002), although a cryptic, sexual generation cannot be ruled out, as cryptic cyclical parthenogenesis has been found in other cynipid species (Abe 2006; Rosenthal and Koehler 1971a). Similarly, oviposition Oxalosuccinic acid has never been recorded in this species, and little is known about the exact placement of eggs on twig tissue. Andricus quercuscalifornicus has been variously divided into different this website subspecies by some authors (Fullaway 1911; Kinsey 1922; Russo 2006; Weld 1957), and, as yet, no molecular genetic information exists about the species. Gall abundance on twigs is correlated with shoot vigor (Rosenthal and Koehler 1971b), but other factors, such as plant genotype, likely determine inter-tree

distributions of galls (Moorehead et al. 1993). Collection of galls and rearing of insects In summer 2007 (June 1–October 10, 2007), 1234 oak apple galls were collected from valley oaks in Davis, Woodland, and Vacaville in the Central Valley of California. Valley oaks were chosen haphazardly from natural stands, riparian areas, suburban areas, and planted groves. All galls were collected from Q. lobata, and at least 20 trees were sampled per site. Galls that had changed from an early green/red to a pale brown/white color, had begun to desiccate, and lacked emergence holes were chosen for the survey. Following collection, each individual gall was placed in a closed clear plastic cup and left outdoors at ambient temperature.