Cereal aphids started to infest cereals in the first week of June and reached their peak in the second and third week of July. They could affect both the quantity and quality of grain yields, but I recommend chemical control only when the aphid population reaches the economic threshold level, which was calculated as 16 aphids/tiller. Pirimicarb is recommended for chemical control, as it controlled aphids efficiently and had a minimal effect on the available predators and parasites. A sequential sampling plan has been developed to detect if populations reach economic threshold. Temperature accumulation, starting from the first detection of aphids on the crop, allowed prediction of the time of peak population on the crop.

No description available.

The linkage relationship and arm location of the gene for greenbug resistance in the variety Will was determined by using primary trisonomics and tertiary trisomic homozygous translocations. The gene for greenbug resistance was found to be on linkage group 1 by using primary trisonomics. The gene was located on the cetromere segment of the Tl-6a translocation by using a tertiary trismoic homozygous for greenbug resistance. The data further substantiates the feasibility of using trisomics in placing genes on proper linkage groups.

Thesis (Ph.D.)--University of Nebraska-Lincoln, 2006. / Title from title screen (site viewed June 8, 2007). PDF text: vii, 114 p. : ill. ; 0.82 Mb. UMI publication number: AAT 3242150. Includes bibliographical references. Also available in microfilm and microfiche formats.

Call number: LD2668 .T4 1978 M67 / Master of Science

Call number: LD2668 .T4 1957 O77 / Master of Science

Greenbug is one of two key insect pests of sorghum, and biotype evolution hinders the long-term usefulness of resistant sorghums. The current study sought to identify plant resistance mechanisms, plant damage characteristics, and greenbug fitness in sorghum/greenbug interactions. Choice tests were conducted to elucidate resistance mechanisms displayed by four sorghum genotypes towards several greenbug biotypes and isolates. Results indicated all three resistance modalities (antibiosis, antixenosis, tolerance) were identified in sorghums, with some genotypes displaying two or more modalities towards some biotypes. This suggests some sorghum genotypes do not select for greenbug biotypes, and the sorghum genotypes cultivated may have relatively long-term resistance. Non-choice tests were used to determine plant damage associated with greenbug feeding. Four sorghum genotype, Johnson grass, and five greenbug biotype combinations were used to elucidate plant characteristics associated with visible plant damage. Fluid loss and plant stunting were significantly associated with visible plant damage, and were also observed in some plants not incurring heavy visible damage. Additionally, some biotypes avirulent to cultivated sorghum caused significant damage to Johnson grass. These results suggest visible plant damage, routinely used in damage studies, reflects underlying causes that could lead to poor agronomic performance. Additionally, Johnson grass may harbor greenbug biotypes not commonly found in sorghum fields. Greenbug colony and individual fitness were determined by reproduction rates of five biotypes on four sorghum genotypes and Johnson grass in non-choice tests. Generally, colony and individual fitness estimates were not different within genotype/biotype combinations. Also, biotypes did best on more susceptible and worst on more resistant sorghum genotypes. Colonies and individuals of all biotypes had lowest fitness on Johnson grass. These results suggest virulent biotypes may have a fitness advantage over avirulent ones, at least in the presence of the cultivated host. The results presented herein reflect the diversity of sorghum/greenbug interactions, and underscore the need for further understanding of the nature of greenbug biotypes, and how they interact with cultivated and non-cultivated host plants.

Greenbug is one of two key insect pests of sorghum, and biotype evolution hinders the long-term usefulness of resistant sorghums. The current study sought to identify plant resistance mechanisms, plant damage characteristics, and greenbug fitness in sorghum/greenbug interactions. Choice tests were conducted to elucidate resistance mechanisms displayed by four sorghum genotypes towards several greenbug biotypes and isolates. Results indicated all three resistance modalities (antibiosis, antixenosis, tolerance) were identified in sorghums, with some genotypes displaying two or more modalities towards some biotypes. This suggests some sorghum genotypes do not select for greenbug biotypes, and the sorghum genotypes cultivated may have relatively long-term resistance. Non-choice tests were used to determine plant damage associated with greenbug feeding. Four sorghum genotype, Johnson grass, and five greenbug biotype combinations were used to elucidate plant characteristics associated with visible plant damage. Fluid loss and plant stunting were significantly associated with visible plant damage, and were also observed in some plants not incurring heavy visible damage. Additionally, some biotypes avirulent to cultivated sorghum caused significant damage to Johnson grass. These results suggest visible plant damage, routinely used in damage studies, reflects underlying causes that could lead to poor agronomic performance. Additionally, Johnson grass may harbor greenbug biotypes not commonly found in sorghum fields. Greenbug colony and individual fitness were determined by reproduction rates of five biotypes on four sorghum genotypes and Johnson grass in non-choice tests. Generally, colony and individual fitness estimates were not different within genotype/biotype combinations. Also, biotypes did best on more susceptible and worst on more resistant sorghum genotypes. Colonies and individuals of all biotypes had lowest fitness on Johnson grass. These results suggest virulent biotypes may have a fitness advantage over avirulent ones, at least in the presence of the cultivated host. The results presented herein reflect the diversity of sorghum/greenbug interactions, and underscore the need for further understanding of the nature of greenbug biotypes, and how they interact with cultivated and non-cultivated host plants.

Digitized by Kansas State University Libraries

Thesis ( MScAgric) -- Stellenbosch University, 1997. / ENGLISH ABSTRACT: Stem rust is considered the most damaging of the wheat rusts causing yield losses of more than 50% in epidemic years. Similarly, Russian wheat aphids (RWA) can be regarded as one ofthe most devastating insect pests of wheat. Yield losses due to R W A primarily result from a reduction in plant resources (sucking plant sap). Secondary losses are incurred by viruses transmitted during feeding. Mapping disease and insect resistance genes that are effective against prevailing pathotypes and biotypes of South Africa will optimize their utilization in breeding programmes. The wheat line, 87M66-2-l, is homozygous for a single dominant stem rust resistance gene located on chromosome lD. This stem rust resistance gene has been derived from Triticum tauschii accession RL5289 and is here referred to as Srtau. The aim of this study was to determine the chromosome arm involved. Following the chromosome arm allocation of Srtau, its possible linkage with the genes Rg2, Lr 21 , Sr X and Sr 33 was studied. A telosomic analysis has shown that Srtau is located on chromosome arm 1 DS and is linked to the centromere with a recombination frequency of 21 ± 3 .40%. Glume blotch and a heavy mildew infection of segregating families planted in the field in 1996 made the linkage study between Lr 21 (leaf rust resistance) and Rg2 (glume colour) impossible. However, estimated linkages of 9 ± 1.9 map units between Sr33 (stem rust resistance) and Srtau, ± 6 map units between Sr X (stem rust resistance) and Sr 3 3 and ± 1 0 map units between Sr X and Srtau suggested that SrX, Sr33 and Srtau are closely linked on I DS. Taking existing map data into consideration, it seems that the most likely order of the genes is: centromere - Srtau - Sr 3 3 - Sr X. A single dominant R W A resistance gene, Dn5, was identified in the T aestivum accession 'SA 463' and is located on chromosome 7D. The aim ofthis study was to determine the chromosome arm involved. The possible linkage of Dn5 with the endopeptidase locus, Ep-D1 b. and chlorina mutant gene, cn-D1, was then studied. Endopeptidase zymograms of 'SA 463' revealed two unknown polymorphisms. F 2 monosomic analyses involving the chromosomes 7 A, 7B and 7D were performed in an attempt to identify the loci associated with these polymorphisms. Dn5 was mapped on chromosome arm 7DL. A recombination frequency of60 ± 4.53% between Dn5 and the centromere suggested the absence of linkage. Linkage between Ep-Dl and cn-Dl could not be calculated as a result of similar isoelectric points of the 7DL encoded endopeptidases of the parental material studied. Recombination frequencies of32 ± 4.97% between Dn5 and EpDl and 37 ± 6.30% between Dn5 and cn-Dl were, however, encountered. The two novel endopeptidase alleles encountered in 'SA 463' were designated as Ep-Dle and Ep-Ald. A RWA resistance gene was transferred from the rye accession ' Turkey 77' to wheat and in the process the RWA resistant wheat lines 91M37-7 and 91M37-51 were derived. No rye chromatin could be detected in these plants following C-banding. The aim of this study was to determine (i) on which chromosome the gene(s) is located, and (ii) whether the resistance can be the result of a small intercalary translocation of rye chromatin. A monosomic analysis of the RWA resistance gene in 91M37-51 has shown that a single dominant resistance gene occurs on chromosome 7D. The use of rye-specific dispersed probes did not reveal any polymorphisms between the negative controls and RW A resistant lines 91M3 7- 7 and 91M37-51 which would suggest that it is unlikely that the resistance was derived from rye. / AFRIKAANSE OPSOMMING: Stamroes word as die mees vemietigende graanroessiekte beskou en het in epidemiese jare oesverliese van meer as 50% tot gevolg. Russiese koringluise is eweneens een van die emstigste insekplae van koring. Russiese koringluise veroorsaak oesverliese deurdat dit plantsap uitsuig en die plant van voedingstowwe beroof. Dit tree egter ook as 'n virusvektor op en kan so indirekte oesverliese veroorsaak. Kartering van siekte- en insekweerstandsgene wat effektief is teen die Suid-Afrikaanse patotipes en biotipes, sal hulle gebruik in teelprogramme optimiseer. Die koringlyn, 87M66-2-l , is homosigoties vir 'n dominante stamroes-weerstandsgeen wat op chromosoom ID voorkom. Hierdie weerstandsgeen is uit die Triticum tauschii aanwins, RL5289, afkomstig en word hiema verwys as Srtau. Daar is gepoog om te bepaal op watter chromosoomarm Srtau voorkom, waama sy koppeling met betrekking tot die gene Rg2, Lr21 , SrX en Sr33 bepaal is. 'n Telosoomanalise het getoon dat Srtau op chromosoom-arm 1 DS voorkom en gekoppel is aan die sentromeer met 'n rekombinasie-frekwensie van 21 ± 3.40%. Segregerende populasies wat in 1996 in die land geplant is, is hewig deur aarvlek en poeieragtige meeldou besmet en dit het die moontlike bepaling van koppeling tussen Lr21 (blaarroesweerstand) en Rg2 (aarkaffie kleur) belemmer. Koppelingsafstande van 9 ± 1. 9 kaart-eenhede tussen Sr 33 (stamroesweerstand) en Srt au, ± 6 kaart -eenhede tussen Sr X ( stamroesweerstand) en Sr 3 3 en ± 1 0 kaart -eenhede tussen SrX en Srtau is geraam en toon dat SrX, Sr33 en Srtau nou gekoppel is. Die waarskynlikste volgorde van die gene op lDS is: sentromeer- Srtau- Sr33- SrX. 'n Enkele dominante Russiese koringluis-weerstandsgeen, Dn5, is in dieT aestivum aanwins 'SA 463 ' ge"identifiseer en kom op chromosoom 7D voor. Die studie het ten doel gehad om te bepaal op watter chromosoom-arm Dn5 voorkom, asook wat die koppeling van Dn5 met die endopeptidase lokus, Ep-Dl, en die chlorina mutante geen, cn-Dl , is. Endopeptidase simograrnme van 'SA 463' het twee onbekende polimorfismes getoon. Die gene wat kodeer vir hierdie twee polimorfismes is met behulp van F2 monosoom-analises wat die chromosome 7 A, 7B en 7D betrek, gei:dentifiseer. Dn5 is op chromosoom 7DL gekarteer. 'n Rekombinasie-frekwensie van 60 ± 4.53% is gevind vir die sentromeer en Dn5 en dui op die afwesigheid van koppeling. Koppeling tussen Ep-Dl en cn-Dl kon nie bepaal word nie omdat die endopeptidase bande geproduseer deur die ouerlike materiaal wat in die studie gebruik is, nie met sekerheid in die nageslag onderskei kon word nie. Rekombinasie-frekwensies van 32 ± 4.97% tussen Dn5 en Ep-Dl en 37 ± 6.30% tussen Dn5 en cn-Dl is egter bereken. Dit word voorgestel dat daar na die twee onbekende endopeptidase-allele wat in 'SA 463 ' voorkom, verwys word as Ep-Dle en Ep-Ald. 'n Russiese koringluis-weerstandsgeen is uit die rog-aanwins, 'Turkey 77', oorgedra na koring en in die proses is die Russies koringluis weerstandbiedende lyne, 91M37-7 en 91M37-51 , geproduseer. Geen rog-chromatien kon egter met behulp van C-bande in hierdie lyne waargeneem word nie. Die doel van die studie was om te bepaal (i) op watter chromosoom die geen(e) voorkom, en (ii), of die Russiese koringluis weerstandsgeen die gevolg kan wees van 'n klein interkalere translokasie van rog- chromatien. 'n Monosoom-analise van die Russiese koringluis-weerstandsgeen in 91M37-51 het getoon dat 'n enkele dominante weerstandsgeen op chromosoom 7D voorkom. Rog-spesifieke herhalende peilers het geen polimorfismes tussen negatiewe kontroles en die Russiese koringluis weerstandbiedende lyne 91M37-7 en 91M37-51 getoon nie. Dit is dus onwaarskynlik dat die weerstand in die lyne uit rog verhaal is.