Molecular markers closely linked to genes that confer a high level of resistance to root-knot nematode (RKN) [Meloidogyne incognita (Kofoid & White) Chitwood] in cotton (Gossypium hirsutum L.) germplasm derived from Auburn 623 RNR would greatly facilitate cotton breeding programs. Our objectives were to identify simple sequence repeat (SSR) markers linked to RKN resistance quantitative trait loci (QTL) and map these markers to specific chromosomes. We developed three recombinant inbred line (RIL) populations by single seed descent from the crosses of RKN-resistant parents M-240 RNR (M240), developed from the Auburn 623 RNR source, moderately resistant Clevewilt 6 (CLW6), one of the parents of Auburn 623 RNR, and susceptible parent Stoneville 213 (ST213). These crosses were CLW6 × ST213, M240 × CLW6, and M240 × ST213. RILs from these populations were grown under greenhouse conditions, inoculated with RKN eggs, scored for root gall index, eggs plant(-1), and eggs g(-1) root. Plants were also genotyped with SSR markers. Results indicated that a minimum of two major genes were involved in the RKN resistance of M240. One gene was localized to chromosome 11 and linked to the marker CIR 316-201. This CIR 316-201 allele was also present in CLW6 but not in Mexico Wild (MW) (PI593649), both of which are parents of Auburn 623 RNR. A second RKN resistance gene was localized to the short arm of chromosome 14 and was linked to the SSR markers BNL3545-118 and BNL3661-185. These two marker alleles were not present in CLW6 but were present in MW. Our data also suggest that the chromosome 11 resistance QTL primarily affects root galling while the QTL on chromosome 14 mediates reduced RKN egg production. The SSRs identified in this study should be useful to select plants with high levels of RKN resistance in segregating populations derived from Auburn 623 RNR.

Inactivation of the water splitting enzyme complex in leaves or isolated chloroplasts results in increased susceptibility of photosystem II (PSII) to damage by light. Photoinhibition under this condition occurs in very weak light. The site of damage is exclusive of the water splitting complex yet still on the oxidizing side of PSII, as the QB locus is unaffected while photoreduction of silicomolybdate is inhibited. The kinetics of loss in PSII activity are more complex than apparent first-order, and the quantum efficiency is low. We observe no evidence of deletion from thylakoid membranes of any PSII polypeptide as a consequence of photoinhibition, although recovery from the photoinhibition is dependent upon both light and 70S protein synthesis. Enhanced synthesis of two proteins occurs during recovery, only one of which (D2) appears to be causally related to the recovery. We present a model which describes the relationship of weak light photoinhibition and its recovery to photoactivation of the S-state water oxidizing complex.Irradiation of oxygenic photosynthetic organisms or their isolated chloroplasts with intense visible light inhibits photosynthesis by poorly understood processes at specific loci in the electron transport sequence and reaction centers (see Refs. 33 and 38 for recent reviews). Such photoinhibitions of photosynthesis proceed via low quantum yield processes following light absorption by Chl (18)

The identification of molecular markers that are closely linked to gene(s) in Gossypium barbadense L. accession GB713 that confer a high level of resistance to reniform nematode (RN), Rotylenchulus reniformis Linford & Oliveira, would be very useful in cotton breeding programs. Our objectives were to determine the inheritance of RN resistance in the accession GB713, to identify SSR markers linked with RN resistance QTLs, and to map these linked markers to specific chromosomes. We grew and scored plants for RN reproduction in the P(1), P(2), F(1), F(2), BC(1)P(1), and BC(1)P(2) generations from the cross of GB713 × Acala Nem-X. The generation means analysis using the six generations indicated that one or more genes were involved in the RN resistance of GB713. The interspecific F(2) population of 300 plants was genotyped with SSR molecular markers that covered most of the chromosomes of Upland cotton (G. hirsutum L.). Results showed two QTLs on chromosome 21 and one QTL on chromosome 18. One QTL on chromosome 21 was at map position 168.6 (LOD 28.0) flanked by SSR markers, BNL 1551_162 and GH 132_199 at positions 154.2 and 177.3, respectively. A second QTL on chromosome 21 was at map position 182.7 (LOD 24.6) flanked by SSR markers BNL 4011_155 and BNL 3279_106 at positions 180.6 and 184.5, respectively. Our chromosome 21 map had 61 SSR markers covering 219 cM. One QTL with smaller genetic effects was localized to chromosome 18 at map position 39.6 (LOD 4.0) and flanked by SSR markers BNL 1721_178 and BNL 569_131 at positions 27.6 and 42.9, respectively. The two QTLs on chromosome 21 had significant additive and dominance effects, which were about equal for each QTL. The QTL on chromosome 18 showed larger additive than dominance effects. Following the precedent set by the naming of the G. longicalyx Hutchinson & Lee and G. aridum [(Rose & Standley) Skovsted] sources of resistance, we suggest the usage of Ren (barb1) and Ren (barb2) to designate these QTLs on chromosome 21 and Ren (barb3) on chromosome 18.

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