Global status of wheat leaf rust caused by Puccinia triticina

Euphytica (Impact Factor: 1.69). 01/2011; 179(1):143-160. DOI: 10.1007/s10681-011-0361-x

ABSTRACT Leaf rust caused by Puccinia triticina is the most common and widely distributed of the three wheat rusts. Losses from leaf rust are usually less damaging than
those from stem rust and stripe rust, but leaf rust causes greater annual losses due to its more frequent and widespread occurrence.
Yield losses from leaf rust are mostly due to reductions in kernel weight. Many laboratories worldwide conduct leaf rust surveys
and virulence analyses. Most currently important races (pathotypes) have either evolved through mutations in existing populations
or migrated from other, often unknown, areas. Several leaf rust resistance genes are cataloged, and high levels of slow rusting
adult plant resistance are available in high yielding CIMMYT wheats. This paper summarizes the importance of leaf rust in
the main wheat production areas as reflected by yield losses, the complexity of virulence variation in pathogen populations,
the role cultivars with race-specific resistance play in pathogen evolution, and the control measures currently practiced
in various regions of the world.

Triticum aestivum

Triticum turgidum

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    ABSTRACT: In wheat, advantageous gene-rich or pleiotropic regions for stripe, leaf, and stem rust and epistatic interactions between rust resistance loci should be accounted for in plant breeding strategies. Leaf rust (Puccinia triticina Eriks.) and stripe rust (Puccinia striiformis f. tritici Eriks) contribute to major production losses in many regions worldwide. The objectives of this research were to identify and study epistatic interactions of quantitative trait loci (QTL) for stripe and leaf rust resistance in a doubled haploid (DH) population derived from the cross of Canadian wheat cultivars, AC Cadillac and Carberry. The relationship of leaf and stripe rust resistance QTL that co-located with stem rust resistance QTL previously mapped in this population was also investigated. The Carberry/AC Cadillac population was genotyped with DArT(®) and simple sequence repeat markers. The parents and population were phenotyped for stripe rust severity and infection response in field rust nurseries in Kenya (Njoro), Canada (Swift Current), and New Zealand (Lincoln); and for leaf rust severity and infection response in field nurseries in Canada (Swift Current) and New Zealand (Lincoln). AC Cadillac was a source of stripe rust resistance QTL on chromosomes 2A, 2B, 3A, 3B, 5B, and 7B; and Carberry was a source of resistance on chromosomes 2B, 4B, and 7A. AC Cadillac contributed QTL for resistance to leaf rust on chromosome 2A and Carberry contributed QTL on chromosomes 2B and 4B. Stripe rust resistance QTL co-localized with previously reported stem rust resistance QTL on 2B, 3B, and 7B, while leaf rust resistance QTL co-localized with 4B stem rust resistance QTL. Several epistatic interactions were identified both for stripe and leaf rust resistance QTL. We have identified useful combinations of genetic loci with main and epistatic effects. Multiple disease resistance regions identified on chromosomes 2A, 2B, 3B, 4B, 5B, and 7B are prime candidates for further investigation and validation of their broad resistance.
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    ABSTRACT: Since weather has a major influence on the occurrence and development of crop diseases, valuable insight toward future agricultural planning emerges with assessment tools to evaluate fungal disease pressure and crop regional suitability under projected future climatic conditions. The aim of this study was to develop two climatic indicators, the average infection efficiency (AIE) and the number of infection days (NID), to quantify the potential effects of weather on the intensity and occurrence of pathogen infection. First, a simple and continuous infection function accounting for daily temperature and leaf wetness duration variations was implemented. The function was then parameterized from published data sets for five major contrasting fungal diseases affecting crops in Northern France: phoma of oilseed rape, late blight of potato, downy mildew of grape, leaf rust of wheat and net blotch of barley. Finally, AIE and NID were calculated for the recent past (1970–2000) and the future A1B climate scenario (2070–2100). An overall decrease in the risk of infection was shown for potato late blight and downy mildew of grapevine for all months during the period when the host plant is susceptible to infection. There were greater differences for the other three diseases, depending on the balance between warmer temperatures and lower humidity. The future climate would result in a later onset of disease and higher infection pressure in late autumn. In spring, for brown rust of wheat and net blotch of barley, the climatic risk for infection is expected to occur earlier but would result in lower infection pressure in May. These findings highlighted the need to use an infra-annual (monthly or seasonally) scale to achieve a relevant analysis of the impact of climate change on the infection risk. The described indicators can easily be adapted to other pathogens and may be useful for agricultural planning at the regional scale and in the medium term, when decision support tools are required to anticipate future trends and the associated risks of crop diseases.
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    ABSTRACT: To confirm allelic relationship between Lr9 and the leaf rust resistance gene in KLM4-3B, genetics of resistance was studied using crosses (WL711 + Lr9) × WL711 and (WL711 + LrKLM4-3B) × WL711. The F 2 populations in cross (WL711 + Lr9) × WL711 and (WL711 + LrKLM4-3B) × WL711 segregated in ratio of 3:1 for disease reaction at seed-ling stage against pathotype 77-5 of leaf rust. This suggests that rust resistance in these stocks are under the control of single dominant genes. Further, to study allelic relationship between Lr9 and LrKLM4-3B, F 2 population of the cross (WL711 + LrKLM4-3B) × (WL711 + Lr9) was studied. A segregation ratio of 15:1 implies that the two genes Lr9 and LrKLM4-3B are non-allelic genes.


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May 20, 2014