Biological Control of Fenusa pusilla (Hymenoptera: Tenthredinidae) in the Northeastern United States: A Thirty-four Year Perspective on Efficacy

Parasitoid releases against the birch leafminer Fenusa pusilla (Lepeletier) (Hymenoptera: Tenthredinidae) in eastern North America began in 1974, with releases in eastern Canada, followed by others in the Middle Atlantic States and New England. Of 4 parasitoids released, only 1, the ichneumonid Lathrolestes nigricollis (Thompson), established and spread widely. Studies of its preliminary impacts were made in several locations in the 1980s and 1990s, but full impact of the parasitoid on host density was not yet achieved in that period. Here we report results of surveys in 7 states (MA, CT, RI, NY, PA, NJ, DE) in 2007 documenting the current birch leaf miner levels (as % of leaves mined in spring) and parasitism. Survey results show that the pest has declined dramatically to barely detectable levels in 5 states (MA, CT, RI, NY, PA) but that in southern NJ, the pest remains abundant (ca 50% leaves mined) despite significant parasitism levels. Survey results, in context with previous evaluations made when populations were still declining, show that the project has been completely successful in much of the northeastern USA, but that there is a southern limit to efficacy in mid-New Jersey. Possible reasons for lack of control in this area, in contrast to high levels of control elsewhere, are discussed

Effects of di(n-butyl) phthalate exposure on foetal rat germ-cell number and differentiation: identification of age-specific windows of vulnerability: DBP effects on foetal germ cells

Environmental factors are implicated in increased incidence of human testicular germ‐cell cancer (TGCC). TGCC has foetal origins and may be one component of a testicular dysgenesis syndrome (TDS). Certain phthalates induce TDS in rats, including effects on foetal germ cells (GC). As humans are widely exposed to phthalates, study of the effects of phthalates on foetal rat GC could provide an insight into the vulnerability of foetal GC to disruption by environmental factors, and thus to origins of TGCC. This study has therefore characterized foetal GC development in rats after in utero exposure to di(n‐butyl) phthalate (DBP) with emphasis on GC numbers/proliferation, differentiation and time course for inducing effects. Pregnant rats were treated orally from embryonic day 13.5 (e13.5) with 500 mg/kg/day DBP for varying periods. GC number, proliferation, apoptosis, differentiation (loss of OCT4, DMRT1 expression, DMRT1 re‐expression, GC migration) and aggregation were evaluated at various foetal and postnatal ages. DBP exposure reduced foetal GC number by ∼60% by e15.5 and prolonged GC proliferation, OCT4 and DMRT1 immunoexpression; these effects were induced in the period immediately after testis differentiation (e13.5–e15.5). In contrast, DBP‐induced GC aggregation stemmed from late gestation effects (beyond e19.5). Foetal DBP exposure delayed postnatal resumption of GC proliferation, leading to bigger deficits in numbers, and delayed re‐expression of DMRT1 and radial GC migration. Therefore, DBP differentially affects foetal GC in rats according to stage of gestation, effects that may be relevant to the human because of their nature (OCT4, DMRT1 effects) or because similar effects are demonstrable in vitro on human foetal testes (GC number). Identification of the mechanisms underlying these effects could give a new insight into environment‐sensitive mechanisms in early foetal GC development that could potentially be relevant to TGCC origins

Distribution of \u3cem\u3eCotesia rubecula\u3c/em\u3e (Hymenoptera: Braconidae) and Its Displacement of \u3cem\u3eCotesia glomerata\u3c/em\u3e in Eastern North America

A survey was conducted from May to Oct of 2011 of the parasitoid community of the imported cabbageworm, Pieris rapae (Lepidoptera: Pieridae), in cole crops in part of the eastern United States and southeastern Canada. The findings of our survey indicate that Cotesia rubecula (Hymenoptera: Braconidae) now occurs as far west as North Dakota and has become the dominant parasitoid of P. rapae in the northeastern and north central United States and adjacent parts of southeastern Canada, where it has displaced the previously common parasitoid Cotesia glomerata (Hymenoptera: Braconidae). Cotesia glomerata remains the dominant parasitoid in the mid-Atlantic states, from Virginia to North Carolina and westward to southern Illinois, below latitude N 38° 48′. This pattern suggests that the released populations of C. rubecula presently have a lower latitudinal limit south of which they are not adapted

Microscopic analysis of the microbiota of three commercial Phytoseiidae species (Acari: Mesostigmata)

Microbes associated with the external and internal anatomy of three commercially available predatory mite species, Phytoseiulus persimilis, Typhlodromips (=Amblyseius) swiskii, and Neoseiulus (=Amblyseius) cucumeris were examined using light microscopy, confocal laser scanning microscopy and fluorescence in-situ hybridization (FISH). Four microbe morphotypes were observed on external body regions. These included three microfungi-like organisms (named T1, T2 and T3) and rod-shaped bacteria (T4). Morphotypes showed unique distributions on the external body regions and certain microbes were found only on one host species. Microfungi-like T1 were present in all three species whereas T2 and T3 were present in only P. persimilis and T. swirskii respectively. T1 and T2 microbes were most abundant on the ventral structures of the idiosoma and legs, most frequently associated with coxae, coxal folds, ventrianal shields and epigynal shields. T3 microbes were most abundant on legs and dorsal idiosoma. T4 microbes were less abundant and were attached to epigynal shields of N. cucumeris and T. swirskii. Significant differences in distribution between seasons (spring and winter) suggest that there are fluctuations in the microbiota of phytoseiids in mass reared systems. FISH using the EUB338 (I-III) probes showed bacteria within the alimentary tract, in Malpighian tubules and anal atria. It is possible these have a role in absorbing excretory products or maintaining gut physiology. We suggest how microbes might be transmitted to offspring and throughout populations. The implications of these findings for commercial mass rearing are discussed. This study highlights the necessity of understanding the intrinsic microbiota of Phytoseiidae and other Acari

Fetal programming of adult Leydig cell function by androgenic effects on stem/progenitor cells

status: publishe

Differential gene expression in human granulosa cells from recombinant FSH versus human menopausal gonadotropin ovarian stimulation protocols

<p>Abstract</p> <p>Background</p> <p>The study was designed to test the hypothesis that granulosa cell (GC) gene expression response differs between recombinant FSH and human menopausal gonadotropin (hMG) stimulation regimens.</p> <p>Methods</p> <p>Females < 35 years-old undergoing IVF for tubal or male factor infertility were prospectively randomized to one of two stimulation protocols, GnRH agonist long protocol plus individualized dosages of (1) recombinant (r)FSH (Gonal-F) or (2) purified human menopausal gonadotropin (hMG; Menopur). Oocytes were retrieved 35 h post-hCG, and GC were collected. Total RNA was extracted from each GC sample, biotinylated cRNA was synthesized, and each sample was run on Human Genome Bioarrays (Applied Microarrays). Unnamed genes and genes with <2-fold difference in expression were excluded.</p> <p>Results</p> <p>After exclusions, 1736 genes exhibited differential expression between groups. Over 400 were categorized as signal transduction genes, ~180 as transcriptional regulators, and ~175 as enzymes/metabolic genes. Expression of selected genes was confirmed by RT-PCR. Differentially expressed genes included A kinase anchor protein 11 (AKAP11), bone morphogenetic protein receptor II (BMPR2), epidermal growth factor (EGF), insulin-like growth factor binding protein (IGFBP)-4, IGFBP-5, and hypoxia-inducible factor (HIF)-1 alpha.</p> <p>Conclusions</p> <p>Results suggest that major differences exist in the mechanism by which pure FSH alone versus FSH/LH regulate gene expression in preovulatory GC that could impact oocyte maturity and developmental competence.</p

Proposed Role for COUP-TFII in Regulating Fetal Leydig Cell Steroidogenesis, Perturbation of Which Leads to Masculinization Disorders in Rodents

Reproductive disorders that are common/increasing in prevalence in human males may arise because of deficient androgen production/action during a fetal ‘masculinization programming window’. We identify a potentially important role for Chicken Ovalbumin Upstream Promoter-Transcription Factor II (COUP-TFII) in Leydig cell (LC) steroidogenesis that may partly explain this. In rats, fetal LC size and intratesticular testosterone (ITT) increased ∼3-fold between e15.5-e21.5 which associated with a progressive decrease in the percentage of LC expressing COUP-TFII. Exposure of fetuses to dibutyl phthalate (DBP), which induces masculinization disorders, dose-dependently prevented the age-related decrease in LC COUP-TFII expression and the normal increases in LC size and ITT. We show that nuclear COUP-TFII expression in fetal rat LC relates inversely to LC expression of steroidogenic factor-1 (SF-1)-dependent genes (StAR, Cyp11a1, Cyp17a1) with overlapping binding sites for SF-1 and COUP-TFII in their promoter regions, but does not affect an SF-1 dependent LC gene (3β-HSD) without overlapping sites. We also show that once COUP-TFII expression in LC has switched off, it is re-induced by DBP exposure, coincident with suppression of ITT. Furthermore, other treatments that reduce fetal ITT in rats (dexamethasone, diethylstilbestrol (DES)) also maintain/induce LC nuclear expression of COUP-TFII. In contrast to rats, in mice DBP neither causes persistence of fetal LC COUP-TFII nor reduces ITT, whereas DES-exposure of mice maintains COUP-TFII expression in fetal LC and decreases ITT, as in rats. These findings suggest that lifting of repression by COUP-TFII may be an important mechanism that promotes increased testosterone production by fetal LC to drive masculinization. As we also show an age-related decline in expression of COUP-TFII in human fetal LC, this mechanism may also be functional in humans, and its susceptibility to disruption by environmental chemicals, stress and pregnancy hormones could explain the origin of some human male reproductive disorders