Skip to main content
ARS Home » Southeast Area » Mississippi State, Mississippi » Crop Science Research Laboratory » Genetics and Sustainable Agriculture Research » Research » Publications at this Location » Publication #369186

Research Project: Improvement of Cotton through Genetic Base Diversification and Enhancement of Agronomic, Fiber, and Nematode Resistance Traits

Location: Genetics and Sustainable Agriculture Research

Title: Differential effects of cotton root-knot nematode resistance QTL on RKN development and fecundity

item Wubben, Martin
item Gaudin, Amanda
item McCarty, Jack
item Jenkins, Johnie

Submitted to: Phytopathology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 12/27/2019
Publication Date: 3/2/2020
Citation: Wubben, M., Gaudin, A.G., Mccarty Jr, J.C., Jenkins, J.N. 2020. Differential effects of cotton root-knot nematode resistance QTL on RKN development and fecundity. Phytopathology. 110:927-932.

Interpretive Summary: Resistance of Upland cotton to the southern root-knot nematode (RKN) is controlled by two major quantitative resistance loci (QTL). These QTL are located on chromosomes 11 (CHR11) and 14 (CHR14). In cotton lines that have both QTL, it has been shown that CHR11 and CHR14 affect RKN infection and reproduction in different ways; however, to fully understand these phenomena it is necessary to evaluate the effects of CHR11 and CHR14 when they are by themselves and not combined in a single cotton line. We developed near isolines that were susceptible to RKN, expressed CHR11 alone, expressed CHR14 alone, or carried both QTL. We then evaluated RKN reproduction, post-infection development, egg mass formation, and RKN female fecundity for each isoline. Our experiments demonstrate that CHR11 has an immediate effect on the RKN lifecycle by inhibiting the ability of the infective RKN juvenile to develop into later juvenile and adult stages. In contrast, RKN development in CHR14 plants is normal until around 21 days after inoculation at which point the nematode is unable to complete its development and become a mature adult female. In addition, RKN that fully mature on CHR14 plants produce significantly eggs than females that develop on susceptible and CHR11 plants. These findings show that the CHR11 and CHR14 resistance loci effect resistance via different mechanisms and are additive in their impact when combined into a single cotton line.

Technical Abstract: Upland cotton (Gossypium hirsutum) resistance to the southern root-knot nematode (RKN) (Meloidogyne incognita) is controlled by quantitative trait loci (QTL) on chromosomes 11 and 14. The individual contributions of these QTL, referred to as qMi-C11 (CHR11) and qMi-C14 (CHR14), to the resistance phenotype are not well understood. Here, we describe the development and characterization of near isolines susceptible at both loci, isolines having CHR11 or CHR14 alone, and isolines carrying both QTL (CHR11/CHR14). Total RKN reproduction and temporal analyses of post-penetration RKN development, egg mass formation, and female fecundity were evaluated. Total RKN reproduction, measured 6-weeks post inoculation, was reduced to a greater extent in CHR14 versus CHR11 isolines but not as great as when the QTL were combined. Second-stage juvenile (J2) development to the J3 and J4 (J3+J4) life stages was delayed in CHR11 isolines; whereas, the J2 transition to the J3+J4 in CHR14 followed a similar track as in the susceptible null isoline. Further development of J3+J4 nematodes to adult females was inhibited in CHR14 isolines beginning at 21 days after inoculation (DAI). Total adult female numbers were significantly decreased in CHR11 and CHR14 isolines at 21 and 28 DAI with CHR11/CHR14 isolines showing an even greater reduction by 28 DAI. The number of egg masses g-1 root (f.w.) at 21, 28, and 35 DAI formed on CHR11 and CHR14 isolines followed a similar track as numbers of adult females at these time-points. RKN fecundity (eggs/egg mass) was reduced for CHR11 and CHR14 compared to the null at 21 DAI; however, CHR11 eggs/egg mass was only slightly reduced versus the null by 28 DAI. In contrast, CHR14 eggs/egg mass was like CHR11/CHR14, showing a four-fold decrease in eggs/egg mass compared to CHR11 and the null isolines. Our data demonstrate that both CHR11 and CHR14 reduce overall RKN female numbers by different mechanisms, i.e., CHR11 inhibits J2 establishment and subsequent development, whereas CHR14 compromises J3+J4 development to the adult stage. CHR14 also significantly affects RKN female fecundity. The CHR11 and CHR14 resistant QTL impart resistance through different mechanisms and are additive in their effects when combined into a single isoline.