|Roberts, Philip - UNIVERSITY OF CALIFORNIA|
Submitted to: Crop Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 9/28/2009
Publication Date: 5/5/2010
Citation: Roberts, P.A., Ulloa, M. 2010. Introgression of root-knot nematode resistance into tetraploid cottons. Crop Sci. 50 (3):940-951.
Interpretive Summary: The southern root-knot nematode is a soil-inhabiting worm that attacks plant roots. This worm, in combination with the fungus causing Fusarium wilt, severely reduces cotton yields in some growing regions of the U.S. Host-plant resistance is a mechanism by which some cotton varieties withstand or avoid injury by the nematode. This resistance represents an economical and effective method for preventing nematode-induced crop loss. Molecular markers, which are small pieces of DNA that can be detected chemically, are powerful tools for identifying nematode-resistant cottons. To better understand the genetic basis and possible origin of host-plant resistance for the root-knot nematode, we compared the three major resistant cotton sources (Acala NemX, Clevewilt 6, and Auburn 623 RNR) to a diverse array of cultivated and wild cottons using selected molecular markers and DNA sequence information. As expected, root injury in the set of resistant varieties was low compared with that in susceptible varieties. No consistent differences were observed among the resistant varieties at the molecular marker or DNA sequence level. The molecular marker and DNA sequence information suggested that the origin of root-knot nematode resistance in modern cottons was wild cottons from Asia and America, and that this resistance was transferred to cultivated cotton during early breeding efforts. This research provides valuable insights into the origin of root-knot nematode resistance in cotton that will speed the development and release of resistant cotton varieties.
Technical Abstract: The introgression of root-knot nematode (RKN) resistance into tetraploid cotton (Gossypium ssp.) and its ancestral genome origin were examined. Three major germplasm sources (Acala NemX, Clevewilt 6, and Auburn 623 RNR) of RKN resistance were compared with diverse germplasm using selected SSR markers from chromosomes 7, 11 and 14, and DNA sequence information. RKN resistance was evaluated in a total of 56 cotton entries. Differences (P < 0.05) were observed for mean galling index (GI, scale 0 - 10) between the resistant and susceptible entries. GI in the set of resistant germplasm sources ranged from 0.3 (Auburn 634 RNR) to 2.9 (Clevewilt 6), with resistant Acala NemX averaging 1.2. No consistent differences were observed in these three major germplasm sources at allele-marker or DNA sequence level. Except for the SSR CIR316 allele (206 - 207 bp) marker, no alleles from other SSRs were observed on evaluated RKN resistant entries (GI < 3). Allotetraploid Acala and Upland [G. hirsutum L. (AD1)] and Pima [G. barbadense L. (AD2)] cottons showing the same SSR marker amplification alleles as G. arboreum L. (A2) might suggest that RKN resistance was introduced from the diploid cotton A2 genome (genetic distance ranging from 0.19 to 0.27). However, percentage identity from MUCS088 and CIR316 DNA sequences revealed that the Pima cottons and Upland RKN resistant cottons (206 -207 bp) were not only close to A2 but also to G. herbaceum L. (A1), G. thurberi Todaro (D1), and G. trilobum Moncino and Sesse ex DC. (D8) diploid species. Other G. hirsutum DNA sequences were closer to G. raimondii Ulbrich (D5). The SSRs and DNA sequence analyses indicated that the introgression of RKN resistance into G. hirsutum allotetraploid cottons occurred by artificial hybridization with ancestral genome origin from G. arboreum as well as G. thurberi, and not during cotton genome evolution.