Distinct Quantitative Trait Loci Research Articles

Genetics of Seed Abortion and Reproductive Traits in Soybean

In soybean [Glycine max (L.) Merr.], yield or seed number is determined by the number of seeds per pod, the number of pods per plant, and the number of plants per row. Seeds per pod is a function of the number of ovules per pod and the success of seed set (lack of seed abortion). The objective of this study was to define the genetic basis for seed set. In this study, recombinant inbred (RI) segregants of soybean have been used to identify genetic components, quantitative trait loci (QTLs) that regulate different parameters of seed set. The numbers of ovules per pod and abortions were measured in RI segregants of soybean, as were positions and developmental stages of abortions within pods. Quantitative trait loci were identified from segregants of the Minsoy-Noir 1 RI population grown in Utah and Minnesota. These were confirmed in Minsoy-Archer or Noir 1-Archer RI populations grown in Minnesota. The average abortion frequency in the three RI populations ranged from 10 to 29%. Abortions occurred most frequently in the basal position of the pod and embryo development ceased most often at one of two developmental stages: embryos failed to develop (or ovules were not fertilized), or embryos were partially developed and ceased growth just after cotyledon differentiation. Quantitative trait loci were found on several linkage groups, including U11, U13, and U22. The QTLs in U11 were linked to QTLs for flowering date, reproductive period (RP), and maturity. Two separate QTLs on U13 were linked to genes for male and female sterility (Msl, Ms6, or St5) and to genes for disease resistance, respectively. One of two distinct QTLs on U22 was associated with a previously identified QTL for water use efficiency. Also of interest was a QTL on U3 linked to Lfl that determined the number of ovules per pod, suggesting a common regulation of leaf and flower primordia.

Genetics of Seed Abortion and Reproductive Traits in Soybean

In soybean [Glycine max (L.) Merr.], yield or seed number is determined by the number of seeds per pod, the number of pods per plant, and the number of plants per row. Seeds per pod is a function of the number of ovules per pod and the success of seed set (lack of seed abortion). The objective of this study was to define the genetic basis for seed set. In this study, recombinant inbred (RI) segregants of soybean have been used to identify genetic components, quantitative trait loci (QTLs) that regulate different parameters of seed set. The numbers of ovules per pod and abortions were measured in RI segregants of soybean, as were positions and developmental stages of abortions within pods. Quantitative trait loci were identified from segregants of the Minsoy-Noir 1 RI population grown in Utah and Minnesota. These were confirmed in Minsoy-Archer or Noir 1-Archer RI populations grown in Minnesota. The average abortion frequency in the three RI populations ranged from 10 to 29%. Abortions occurred most frequently in the basal position of the pod and embryo development ceased most often at one of two developmental stages: embryos failed to develop (or ovules were not fertilized), or embryos were partially developed and ceased growth just after cotyledon differentiation. Quantitative trait loci were found on several linkage groups, including U11, U13, and U22. The QTLs in U11 were linked to QTLs for flowering date, reproductive period (RP), and maturity. Two separate QTLs on U13 were linked to genes for male and female sterility (Ms1, Ms6, or St5) and to genes for disease resistance, respectively. One of two distinct QTLs on U22 was associated with a previously identified QTL for water use efficiency. Also of interest was a QTL on U3 linked to Lf1 that determined the number of ovules per pod, suggesting a common regulation of leaf and flower primordia.

Multiple blood pressure QTL on rat Chromosome 2 defined by congenic Dahl rats

Linkage analysis previously demonstrated a blood pressure quantitative trait locus (QTL) on rat Chromosome 2 (Chr 2) in crosses utilizing Dahl salt-sensitive (S) rats. The present work dissects this QTL by using congenic strains in which segments of Chr 2 from Wistar Kyoto rats (WKY) are placed on the S genetic background. Two distinct QTLs were found where one QTL was anticipated. These each accounted for a blood pressure of 15-20 mm Hg in rats fed 2% NaCl diet for 24 days. One QTL was in the <9-cM interval between D2Rat35 and D2Wox18 (Fgg), and the other was in the <7-cM interval between D2Wox18 (Fgg) and D2Mgh10. A third tentative QTL was suggested, but not clearly established, in the <3-cM interval between D2Mgh10 and D2Rat259.

QTL analysis reveals different and independent modes of inheritance for diagnostic achene characters in Microseris (Asteraceae)

There are few reliable diagnostic morphological characters for species of the asteracean genus Microseris, and quantitative differences in the shapes of the achenes and the paleaceous pappus parts play a decisive role in species recognition. The genetic basis of species and strain differences in various characters has been studied previously, but little is known about quantitative characters of the achenes. We performed a quantitative trait locus (QTL) analysis in the F2 of an interspecific cross between Microseris douglasii and M. bigelovii for achene length, achene diameter, achene shape, palea length, awn length, and achene pigmentation. Independent inheritance of the main heritable achene characters – achene length, palea length and achene pigmentation – was revealed by the detection of distinct and specific QTLs for these characters. For palea length five QTLs with about equal phenotypic effects were mapped on four different linkage groups. Achene length and achene shape (achene length / achene diameter) were determined by two different genetic systems with one major gene and two modifiers. The detection of QTLs with a polarity of the effects opposite to that in the parental strains for achene length and achene shape reveals genetic variation for a potential increase in species differences. For the highly heritable trait, achene pigmentation, the bimodal F2 distribution suggested single-factor inheritance for absence versus presence of spots, with dominance for the spotted condition. However, only relatively weak QTL effects on that trait could be detected. Additional molecular markers (RAPDs, AFLPs) have to be tested for cosegregation with that major gene. The results are discussed in the context of different theories for the evolution of morphological characters.

Genetic control of susceptibility to experimental Lyme arthritis is polygenic and exhibits consistent linkage to multiple loci on chromosome 5 in four independent mouse crosses.

C3H/He mice infected with Borrelia burgdorferi develop severe arthritis and are high antibody responders, while infected C57BL/6 and BALB/c mice develop mild arthritis and less robust humoral responses. Genetic analysis using composite interval mapping (CIM) on reciprocal backcross populations derived from C3H/HeN and C57BL/6N or C3H/HeJ and BALB/cAnN mice identified 12 new quantitative trait loci (QTL) linked to 10 murine Lyme disease phenotypes. These QTL reside on chromosomes 1, 2, 4, 6, 7, 9, 10, 12, 14, 15, 16, and 17. A reanalysis of an F(2) intercross between C57BL/6N and C3H/HeN mice using CIM identified two new QTL on chromosomes 4 and 15 and confirmed the location of seven previously identified loci. Two or more experimental crosses independently verified six QTL controlling phenotypes after B. burgdorferi infection. Additionally, Bb2 on chromosome 5 was reproduced in four experimental populations and was linked to the candidate locus Cora1. Evidence of four distinct QTL residing within the 30-cM region of chromosome 5 encompassing the previously mapped Bb2 and Bb3 loci was shown by CIM. Interestingly, some alleles contributing to susceptibility to Lyme arthritis were derived from C57BL/6N and BALB/cAnN mice, showing that disease-resistant strains harbor susceptibility alleles.

Quantitative trait loci controlling allergen-induced airway hyperresponsiveness in inbred mice.

Identification of the genetic loci underlying asthma in humans has been hampered by variability in clinical phenotype, uncontrolled environmental influences, and genetic heterogeneity. To circumvent these complications, the genetic regulation of asthma-associated phenotypes was studied in a murine model. We characterized the strain distribution patterns for the asthma-related phenotypes airway hyperresponsiveness (AHR), lung eosinophils, and ovalbumin (OVA)-specific serum immunoglobulin (Ig) E induced by allergen exposure protocols in A/J, AKR/J, BALB/cJ, C3H/HeJ, and C57BL/6J inbred strains and in (C3H/HeJ x A/J)F1 mice. Expression of AHR differed between strains and was sometimes discordant with lung eosinophils or serum IgE. Furthermore, we identified two distinct quantitative trait loci (QTL) for susceptibility to allergen-induced AHR, Abhr1 (allergen-induced bronchial hyperresponsiveness) (lod = 4. 2) and Abhr2 (lod = 3.7), on chromosome 2 in backcross progeny from A/J and C3H/HeJ mice. In addition, a QTL on chromosome 7 was suggestive of linkage to this trait. These QTL differ from those we have previously found to control noninflammatory AHR in the same crosses. Elucidation of the genes underlying these QTL will facilitate the identification of biochemical pathways regulating AHR in animal models of asthma and may provide insights into the pathogenesis of human disease.