Plant-parasitic Nematodes Associated with Grasses Grown for Seed in the Willamette Valley of Oregon.

Plant-parasitic nematodes (PPN) are an understudied pathogen group in the Oregon cool-season grass seed cropping system. In this survey, the PPN associated with annual ryegrass, bentgrass, fine fescue, orchardgrass, perennial ryegrass, and tall fescue were determined. Thirty-seven fields were sampled in the 2022 or 2023 growing season by collecting 10 soil cores in each of six 100-m transects for nematode extraction and visual identification. PerMANOVA testing indicated significant differences in PPN community composition across grass host and sampling time. Pratylenchus and Meloidogyne were the most commonly encountered nematodes, with maximum population densities of 1,984 and 2,496 nematodes/100 g soil, respectively. Sequencing of the COX1 gene region indicated the presence of P. crenatus, P. fallax, P. neglectus, P. penetrans, and P. thornei, with some of these species being detected for the first time on these grass hosts. The only Meloidogyne sp. found in these grasses was M. nassi, based upon sequencing of the ITS gene region. This first-of-its-kind survey indicates the need for further assessment of the impact of these PPNs on yield and stand longevity in cool-season grass seed fields in Oregon.

Ft1, a novel gene related to ubiquitin-conjugating enzymes, is deleted in the Fused toes mouse mutation.

The dominant mouse mutation Fused toes is characterized by partial syndactyly of the limbs and thymic hyperplasia. Both morphological abnormalities were shown to be related to impaired regulation of programmed cell death. Ft/Ft embryos die in midgestation showing severe malformations of fore- and midbrain as well as randomized situs. In Ft mice a large chromosomal deletion (about 300 kb) occurred after insertional mutagenesis. In this report we describe the identification of the first gene that has been mutated by Fused toes. The expression of the novel gene Ft1 is reduced in Ft/+ mice and completely absent in Ft/Ft embryos. Analysis of the Ft1 cDNA revealed an open reading frame that could code for a 32-kDa protein with similarities to ubiquitin-conjugating enzymes. Ft1 transcripts with alternative 5' UTR sequences as well as differential usage of polyadenylation sites were found. Interestingly, the 3' parts of the longest Ft1 transcripts are identical to the reverse complement of the 3'-most sequences of the Rb-related p130 gene. Both genes are transcribed in opposite directions and overlap in their 3' UTRs. Despite the close linkage, p130 expression appeared not to be affected by the Ft mutation. In wild type mice, Ft1 expression levels were found to be high in brain, kidney, and testes and detectable in all other adult organs and throughout embryonic development. Finally, we show that Ft1 is conserved among mammals and identify the human homolog.

Insertional mutagenesis in transgenic mice.

Increasing numbers of transgenic mouse lines have resulted in several dozens of mutants created by insertional mutagenesis. The advantages of different vector systems and the problems associated with the analysis of mutations and the cloning of the affected genes are discussed in this review.

Effect of gonadectomy and exogenous sex hormone administration on the concentrations of hepatic oestrogen receptors and hepatic atypical sex hormone binding protein (HASP) in the rat.

The concentrations of hepatic oestrogen receptors and atypical sex hormone-binding protein are regulated by sex hormones in different manners. Ovariectomy of female rats leads to a significant increase in the concentration of hepatic oestrogen receptors, which can be reversed following administration of either androgens or oestrogens. No differences are observed between total binding site and unoccupied receptor concentrations. Intact male rats contain significantly lower total binding site concentrations and these are not affected by either testectomy or subsequent androgen administration. However, treatment of male castrates with oestradiol leads to the induction of typical female levels. It is not possible to determine the concentrations of unoccupied receptors in intact or gonadectomized males, or rats of either sex treated with androgens, due to masking by the moderate affinity, high capacity oestradiol binder (hepatic atypical sex hormone-binding protein, HASP). Oestradiol binding to this protein is not affected by testectomy nor subsequent androgen administration, but is reduced pressed following treatment with oestradiol. It is also induced in ovariectomized rats by androgens. Oestradiol binding to this protein can be prevented by inclusion of sodium thiocyanate in the assay buffer, thereby permitting unhindered measurement of the oestrogen receptor concentrations.

Contradictory evidence concerning the "universal" role of growth hormone in the regulation of the enzyme activities of hepatic steroid metabolism.

Recent publications suggest that the sexual dimorphism observed in the activities of enzymes involved in drug and steroid metabolism in rat liver are due to sex-specific differences in the rate of growth hormone release. In this paper we set out to demonstrate that this hypothesis cannot be generalized, but has its limitations. Prepuberal hypophysectomy led to the expected "masculinization" of the activities of cytoplasmic 3 alpha-hydroxysteroid dehydrogenase (3 alpha-HSDH), microsomal 3 alpha-HSDH and microsomal 5 alpha-reductase which could be reversed by continuous infusion of human growth hormone (hGH). However, one activity did not conform to this pattern: cytoplasmic 17 beta-HSDH activity reacted to hypophysectomy with a "feminization" and was completely unaffected by hGH infusion. Moreover, microsomal 3 alpha-HSDH in hypophysectomized rats was "feminized" as efficiently by infusion of ovine prolactin (oPRL) as by hGH. Ablation of the pituitary caused loss of measurable cytoplasmic receptor oestrogen concentrations. The inability of either hypophyseal hormone to cause consistent and significant elevation of oestrogen receptor concentrations is probably due to the early age at which the animals were hypophysectomized.

Antagonistic action of estrogens, flutamide, and human growth hormone on androgen-induced changes in the activities of some enzymes of hepatic steroid metabolism in the rat.

The dose-dependent effects of daily estrogen (estradiol, ethinyl estradiol, diethylstilbestrol) administration on the activities of three hepatic androgen-dependent microsomal enzymes (3 alpha- and 3 beta-hydroxysteroid dehydrogenase and 5 alpha-reductase) in male rats were examined. Antiestrogens were then tested for their ability to block the feminizing action of 10 micrograms estradiol/day on these enzyme activities; nafoxidine and monohydroxytamoxifen were the most effective. The prevention of 5 alpha-dihydrotestosterone-induced changes in these activities in ovariectomized females was investigated. All three estrogens at a dose of 1 microgram blocked the action of 500 micrograms androgen. A similar androgenic blockade was achieved by daily administration of 5 mg flutamide or constant infusion of human GH (5 micrograms/h). Simultaneous administration of 200 micrograms monohydroxytamoxifen prevented the androgen-antagonizing action of estrogens, but not of flutamide nor of GH. Large doses of estrogens have the same repressive effect as androgens on 5 alpha-reductase activity in female castrates. Using the diethylstilbestrol-treated rat as a model, it is demonstrated that this effect can be prevented by antiestrogen, but not by GH. It is concluded that androgens and low doses of estrogens affect these enzyme activities by acting at different levels of central regulation, whereas large doses of estrogens act directly on the liver via hepatic estrogen receptors. These conclusions are corroborated by studies of hepatic estrogen receptor concentrations.