DEVELOPMENT OF MOLECULAR MARKERS FOR SELECTION OF LETTUCE GENOTYPES WITH RESISTANCE TO VERTICILLIUM RACE 1

• Sponsoring Institution: Agricultural Research Service/USDA
• Project Status: ACTIVE
• Funding Source: USDA INHOUSE
• Reporting Frequency: Annual
• Accession No.: 0430107
• Project Start Date: Oct 1, 2015
• Project End Date: Jun 30, 2018
• Program Code: [(N/A)]- (N/A)

Recipient Organization
AGRICULTURAL RESEARCH SERVICE
(N/A)
SALINAS,CA 93905

Performing Department
(N/A)

Non Technical Summary
(N/A)

Animal Health Component

60%

Research Effort Categories

Basic

40%

Applied

60%

Developmental

0%

Classification

Knowledge Area (KA)	Subject of Investigation (SOI)	Field of Science (FOS)	Percent
202	1420	1080	10%
204	1429	1080	10%
211	1430	1080	80%

Knowledge Area
204 - Plant Product Quality and Utility (Preharvest); 211 - Insects, Mites, and Other Arthropods Affecting Plants; 202 - Plant Genetic Resources;

Subject Of Investigation
1430 - Greens and leafy vegetables; 1420 - Melons; 1429 - Cucurbits, other;

Field Of Science
1080 - Genetics;

Keywords

lettuce

molecular

markers

genetics

resistance

verticillium

wilt

Goals / Objectives
Development of molecular markers for selection of lettuce genotypes with resistance to Verticillium race 1.

Project Methods
Verticillium wilt is the disease caused by the soil borne fungus Verticillium dahliae. Verticillium wilt has devastating impacts on crops. Plants are often symptomless until they are near market maturity, when the disease develops quickly and often results in complete yield loss in affected fields. The best long-term control of the disease is based on host resistance. Development of resistant cultivars is most desirable, but the progress in breeding is hindered by very slow and labor intensive field-based testing. To make the breeding process more rapid and economically efficient, we will develop molecular markers that can be used to identify the genotypes with Vr1, the dominant gene for resistance to Verticillium wilt race 1. In addition, we will analyze Vr1 resistance homologs in resistant and susceptible accessions and study their relationship.