The corn leafhopper, Dalbulus maidis (DeLong & Wolcott) (Hemiptera: Cicadellidae), is a vector of three maize, Zea mays L., pathogens that have become limiting factors for maize production in some areas of the Americas. Insect feeding plays an important role in vector acquisition and inoculation of pathogens and hence the disease spread. Thus, we sought to understand the different probing and stylet penetration activities performed by this insect while feeding on maize plants, with the ultimate goal of characterizing potential sources of insect resistance in maize. Using electrical penetration graph technology, six distinct waveforms were characterized and correlated with major probing activities of D. maidis via transmission of corn stunt spiroplasma and excretion of honeydew as markers. Major waveforms comprise stylet pathway (waveform 1), active ingestion in nonsieve elements (waveform 2), nonvascular probing (waveform 3), phloem contact (waveform 4, the X wave), phloem ingestion (waveform 5), and oviposition (waveform 6). Our results support most previous findings with this species, and also indicate that some waveforms (2, 4, and 5) are related to biopotentials generated during probing, as was previously found for other hemipteran species. The most important finding from this work is that D. maidis ingests from phloem sieve elements more frequently and for longer durations than seen in previous research, probably due to longer observation periods used in this study. This work provides basic information relevant to the understanding of probing behavior of D. maidis and to the characterization of potential sources of insect-resistant maize.

No abstract

Southern rust, caused by Puccinia polysora Underw., occurs frequently on corn (Zea mays) grown in subtropical or tropical regions. When conditions are favorable, southern rust also occurs in temperate climates of the central and southern United States although the fungus does not survive on corn crop residue and must be introduced to temperate regions each growing season. Several single, dominant, resistance genes, designated as Rpp genes, convey hypersensitive, chlorotic fleck reactions when challenged with avirulent isolates of P. polysora (1). Rpp resistance prevents or limits the formation of uredinia. The Rpp9 gene has been used successfully in North America in the past 20 years to control southern rust even though the gene has been ineffective in other parts of the world (e.g., Africa and Hawaii) because of the prevalence of virulent races. During the past 3 years, Rpp9 virulence has occurred in the western hemisphere (e.g., Brazil, Mexico, Nebraska, and Texas), but prior to 2008, uredinia were not observed east of the Mississippi River on corn with the Rpp9 gene. A few uredinia were observed on corn with the Rpp9 gene in eastern Nebraska in 2006 and near Victoria, TX in 2007 (W. Dolezal, personal observation). In July of 2008, a virulent isolate of P. polysora was confirmed from Grady County, GA on corn lines with the Rpp9 gene including the original source of this resistance gene, Boesman yellow flint, which is PI 186208 (3). In August of 2008, isolates of P. polysora were collected from severely infected corn hybrids with Rpp9 grown in Macon County, GA. Rust samples from hybrids without Rpp genes also were collected in Burke County, GA where Rpp-resistant corn was asymptomatic. In greenhouse trials, corn lines with and without the Rpp9 gene were inoculated with urediniospores from collections from Burke and Macon counties and Illinois. Rust infection types (1) were scored 18 to 25 days after inoculation. The Macon County isolate produced type 1 and 2 infections (small uredinia surrounded by necrotic or chlorotic tissue) on Oh43Rpp9 and W64aRpp9 and type 4 infections (large, sporulating uredinia) on two versions of a commercial hybrid with and without the Rpp9 gene and on Va59 (which carries an Rpp gene different from Rpp9). The Burke County isolate and an isolate from Illinois collected in 2001 produced type 0 infections (chlorotic flecks) on all of these lines except the non-Rpp version of the commercial hybrid which had a type 4 reaction. To our knowledge, Rpp9-virulent isolates of P. polysora have not been reported from the continental United States for nearly 50 years. In the late 1950s and early 1960s, A. L. Robert (2) collected isolates of P. polysora from throughout the world and observed multiple races on a set of host differentials that is no longer available. A. L. Robert's collection included an isolate from Georgia that was virulent on PI 186208. Commercial hybrids containing the Rpp9 gene may continue to be resistant throughout most of North America if previously common Rpp9-avirulent isolates of P. polysora are prevalent, but those hybrids should be carefully monitored for infection by newly introduced Rpp9-virulent isolates. References: (1) A. L. Hooker. Page 207 in: The Cereal Rusts. Vol. II. Academic Press, San Diego, 1985. (2) A. L. Robert. Phytopathology 52:1010, 1962. (3) A. J. Ullstrup. Phytopathology 55:425, 1965.

No abstract

Corn stunt disease has become a factor limiting maize production in some areas of the Americas in recent years. Although resistant maize genotypes have been developed in the past, this resistance has been unstable over time or in some geographical locations. To better understand disease components that could affect the stability of host resistance, we assessed the genome variability of the etiologic agent, Spiroplasma kunkelii. Isolates were obtained from a number of areas, and characterized molecularly by amplification of several regions of the spiroplasma chromosome and sequencing of specific gene fragments. The degree of polymorphism between isolates of different geographic origins was low, and the level of genomic variability was similar within isolates of different countries. Polymorphism among isolates was found in viral insertions and in the sequence of Skarp, a gene that encodes a membrane protein implicated in attachment to insect cells. The results suggest that the genome composition of this species is highly conserved among isolates. Hence, it is unlikely that the instability of maize resistance is due to generation of new pathotypes of S. kunkelii. Instead, other components of this complex pathosystem could account for the breakdown of resistance.