Impaired fungicide activity in plants blocked in disease resistance signal transduction.

Fungicide action is generally assumed to be dependent on an antibiotic effect on a target pathogen, although a role for plant defense mechanisms as mediators of fungicide action has not been excluded. Here, we demonstrate that in Arabidopsis, the innate plant defense mechanism contributes to the effectiveness of fungicides. In NahG and nim1 (for noninducible immunity) Arabidopsis plants, which normally exhibit increased susceptibility to pathogens, the fungicides metalaxyl, fosetyl, and Cu(OH)2 are much less active and fail to control Peronospora parasitica. In contrast, the effectiveness of these fungicides is not altered in Arabidopsis mutants defective in the ethylene or jasmonic acid signal transduction pathways. Application of the systemic acquired resistance activator benzothiadiazole (BTH) in combination with these fungicides results in a synergistic effect on pathogen resistance in wild-type plants and an additive effect in NahG and BTH-unresponsive nim1 plants. Interestingly, BTH treatment normally induces long-lasting pathogen protection; however, in NahG plants, the protection is transient. These observations suggest that BTH treatment can compensate only partially for an impaired signal transduction pathway and support the idea that pathogen defense mechanisms are under positive feedback control. These observations are strikingly reminiscent of the reduced efficacy of antifungal agents in immunocompromised animals.

Contributions to the history of psychology: CXVI. An oral history of C. Kermit Phelps, an 89-year-old African American clinical psychologist.

In a previous article, the authors presented a brief overview of the findings of four audiotaped interviews with C. Kermit Phelps, an 89-year-old African American who earned a Ph.D. in clinical psychology in 1952 from the University of Kansas. Dr. Phelps, who spent his professional career at the Veterans Administration Hospital in Kansas City, Missouri, also maintained a private clinical practice. The present article provides a comprehensive account of the structured interviews.

Salicylate-independent lesion formation in Arabidopsis lsd mutants.

In many interactions of plants with pathogens, the primary host defense reaction is accompanied by plant cell death at the site of infection. The resulting lesions are correlated with the establishment of an inducible resistance in plants called systemic acquired resistance (SAR), for which salicylic acid (SA) accumulation is a critical signaling event in Arabidopsis and tobacco. In Arabidopsis, the lesions simulating disease (lsd) mutants spontaneously develop lesions in the absence of pathogen infection. Furthermore, lsd mutants express SAR marker genes when lesions are present and are resistant to the same spectrum of pathogens as plants activated for SAR by necrogenic pathogen infection. To assess the epistatic relationship between SA accumulation and cell death, transgenic Arabidopsis unable to accumulate SA due to the expression of the salicylate hydroxylase (nahG) gene were used in crosses with the dominant mutants lsd2 or lsd4. Progeny from the crosses were inhibited for SAR gene expression and disease resistance. However, these progeny retained the spontaneous cell death phenotype similar to siblings not expressing nahG. Because lesions form in the absence of SA accumulation for isd2 and lsd4, a model is suggested in which lesion formation in these two mutants is determined prior to SA accumulation in SAR signal transduction. By contrast, the loss of SAR gene expression and disease resistance in nahG-expressing lsd mutants indicates that these traits are dependent upon SA accumulation in the SAR signal transduction pathway.

Recent advances in systemic acquired resistance research--a review.

Little is known about the signal transduction events that lead to the establishment of the broad-spectrum, inducible plant immunity called systemic acquired resistance (SAR). Salicylic acid (SA) accumulation has been shown to be essential for the expression of SAR and plays a key role in SAR signaling. Hydrogen peroxide has been proposed to serve as a second messenger of SA. However, our results do not support such a role in the establishment of SAR. Further elucidation of SAR signal transduction has been facilitated by the identification and characterization of mutants. The lesions simulating disease (lsd). resistance response mutant class exhibits spontaneous lesions similar to those that occur during the hypersensitive response. Interestingly, some lsd mutants lose their lesioned phenotype when SA accumulation is prevented by expression of the nahG gene (encoding salicylate hydroxylase), thereby providing evidence for a feedback loop in SAR signal transduction. Characterization of a mutant non-responsive to SAR activator treatments has provided additional evidence for common signaling components between SAR and gene-for-gene resistance.

Promoter and operator determinants for fur-mediated iron regulation in the bidirectional fepA-fes control region of the Escherichia coli enterobactin gene system.

The fepA-entD and fes-entF operons in the enterobactin synthesis and transport system are divergently transcribed from overlapping promoters, and both are inhibited by the Fur repressor protein under iron-replete conditions. A plasmid harboring divergent fepA'-phoA and fes-entF'-'lacZ fusions, both under the control of this bidirectional regulatory region, was constructed for the purpose of monitoring changes in expression of the two operons simultaneously. Deletion analysis, site-directed mutagenesis, and primer extension were employed to define both a single promoter governing the expression of fes-entF and two tandemly arranged promoters giving rise to the opposing fepA-entD transcript. A single Fur-binding site that coordinately regulates the expression of all transcripts emanating from this control region was identified by in vitro protection from DNase I nicking. The substitution of one base pair in the Fur recognition sequence relieved Fur repression but did not change the in vitro affinity of Fur for its binding site. Additional mutations in a limited region outside of the promoter determinants for either transcript inhibited expression of both fes and fepA. These observations suggest a mechanism of Fur-mediated regulation in this compact control region that may involve other regulatory components.

Effects of Schistosoma mansoni infection on phagocytosis and killing of Proteus vulgaris in Biomphalaria glabrata hemocytes.

With the use of a fluorescence microassay, in vitro phagocytosis and killing of Proteus vulgaris were measured in hemocytes of NIH albino Biomphalaria glabrata infected with Schistosoma mansoni for 1, 2, 3, or 4 wk. Although hemocytes of infected snails displayed decreased phagocytosis, relative to hemocytes of uninfected snails, at 4 wk postinfection (PI), they exhibited enhanced microbicidal activity at 3 wk PI. No microbicidal activity was detected in the plasma of either infected or uninfected snails.

cDNA cloning and expression of potato polyphenol oxidase.

Polyphenol oxidases (PPOs) of plants are copper metalloproteins which catalyze the oxidation of mono- and o-diphenols to o-diquinones. Although PPOs are believed to be primarily responsible for the deleterious browning of many fruit and vegetable crops and are thought to be involved in plant-pest interactions, direct evidence for these roles is lacking. We report the cloning of two PPO cDNAs from Solanum tuberosum leaves. These cDNAs exhibit 97% and 98% sequence similarity at the DNA and deduced amino acid levels, respectively. Putative copper-binding regions of both cDNAs are very similar to those of mammalian, bacterial and Neurospora tyrosinases. Both leaf PPO cDNAs appear to encode polypeptides which are processed to a mature molecular weight of 57,000. In potato leaves, petioles, roots, and flowers, PPO is encoded by ca. 2 kb transcripts. Leaf PPO mRNA is developmentally regulated and only detectable in young foliage. In contrast, the protein profile of immunologically detectable PPO remains constant from the apical node through the eleventh leaf node.

The NCS3 mutation: genetic evidence for the expression of ribosomal protein genes in Zea mays mitochondria.

A deletion eliminating part of a transcribed region of mitochondrial DNA (mtDNA) has been found in the maize nonchromosomal stripe 3 (NCS3) mutant. This results in the specific loss of a set of three mitochondrial RNAs consisting, in normal plants, of a 4.9 kb transcript, its 1.8 kb intron and the resulting processed mRNA of approximately 2.9 kb. In the NCS3 mitochondrial genome the DNA encoding the putative promoter and 5' end of the affected RNAs is missing. This transcribed region of normal maize mtDNA has been sequenced and the intron splice junction has been determined. The 2.9 kb processed mRNA carries two overlapping open reading frames (ORFs) with predicted amino acid sequences that show similarity to two Escherichia coli ribosomal proteins, S3 (rps3) and L16 (rpl16). The presence of severe stunting and striping in NCS3 plants correlates absolutely with the molecular changes described here. This fact and the impaired ability for mitochondrial protein synthesis by NCS3 plants indicate that one or both of these reading frames are translated to functional ribosomal proteins in normal maize mitochondria.

Seroepidemiology of cholera in Gulf coastal Texas.

Single serum samples from 559 volunteers from a Texas Gulf Coast area were examined for vibriocidal antibody to Vibrio cholerae O1 (biotype El Tor, serotype Inaba) by a microtiter method. Elevated levels of vibriocidal antibody were present in 14% of the subjects. Also, 6.8% of the subjects had elevated levels of antibody to the enterotoxin of V. cholerae O1 by the immunoglobulin G enzyme-linked immunosorbent assay. Recent infection, defined on the basis of elevations in both vibriocidal and antitoxin antibodies, had occurred in 1.3% of the subjects. When subjects who reported Brucella infection, travel to a cholera-endemic area, and/or cholera vaccination within a year of the study were removed from the analysis, a prevalence of recent infection of 0.89% was obtained. Significantly higher titers of vibriocidal antibody were found in those with exposure to seawater (fishermen, shrimpers, merchant marines, and dock workers) than in those without such exposure (P less than 0.005). Furthermore, titers of antitoxin antibody were significantly higher in those who consumed shellfish than in nonconsumers. Finally, titers of vibriocidal antibody were significantly higher in Vietnamese subjects than in non-Vietnamese subjects. The results of this study indicate that an endemic focus of infection with V. cholerae occurs in this area.

Preliminary studies on the use of an oral progestogen to induce oestrus and ovulation in seasonally anoestrous Thoroughbred mares.

Daily oral administration of 30 mg allyl trenbolone (Regumate) for 10 to 15 days to 61 barren, maiden and lactating Thoroughbred mares which were exhibiting either deep anoestrus, shallow anoestrus, prolonged spring oestrus or lactation anoestrus, resulted in 54 mares (88 per cent) showing oestrous behaviour within 8 days, and 51 mares (84 per cent) ovulating within 18 days, after the last dose of compound. Response rate was lowest in mares in deep anoestrus. Of the 38 Regumate-treated mares which were covered during the induced oestrus, 21 (55 per cent) conceived. The practical value of this form of progesterone withdrawal therapy as a method for hastening the onset of the breeding season in Thoroughbred mares is discussed.