Wildlife is imperiled in peri-urban landscapes: threats to arboreal mammals.

Urbanization and deforestation impose severe challenges to wildlife, particularly for forest-living vertebrates. Understanding how the peri-urban matrix impacts their survival is critical for designing strategies to promote their conservation. We investigated the threats faced by brown howler monkeys (Alouatta guariba clamitans) in peri-urban regions of Rio Grande do Sul (RS) and Santa Catarina (SC) states, southern Brazil, by compiling negative interaction events (hereafter NIE) reported over more than two decades. We assessed the major NIEs, their distribution among age-sex classes, and the predictors of NIE-related mortality. After 20+ years of monitoring, we compiled 540 NIEs (RS = 248 and SC = 292). Electrocution by power lines was the most frequent cause of death or injury (37%), followed by dog attack (34%), vehicle collision (17%), and human mistreatment (12%). The occurrence of lethal injuries ranged from 5% to 69% depending on the type of NIE and on which state it occurred in. The overall post-NIE mortality was 56%. Adults of both sexes were the most affected individuals in both study regions. The minimal adequate GLM model explained 83% of the variation in NIE-related mortality. State, NIE type, and age-sex class were the main predictors of mortality. Overall, mortality was lower in SC and higher among adult females than in the other classes. We found that the survival of brown howler monkeys in the forest-urban interface is constrained by both the urban infrastructure and the growing interactions with humans and domestic and stray dogs (Canis familiaris). We propose the placement of aerial bridges, road signs and speed bumps in areas of frequent animal crossing, the sterilization of stray dogs, and the sensitization of local inhabitants on the importance of respecting and protecting wildlife to reduce their NIEs with humans and domestic animals in the forest-urban interface.

[IgG4-related disease: a possible cause of obstructive jaundice]. / La maladie liée aux IgG4: une cause possible d'ictère obstructif.

Immunoglobulin G4 related disease (IgG4-RD) has been recognized since early 2000s as an entity comprising a set of inflammatory diseases with common histopathological features. The disease may affect almost all organs and tissues, and often occurs in a subacute fashion in males over 50 years as a mass or diffuse enlargement of affected organs. The histopathological appearance is characterized by a lymphoplasmacytic infiltration with predominantly IgG4-positive plasma cells and progressive fibrosis. Its clinical and radiological features can make the distinction with a malignancy difficult. The disease responds well to systemic glucocorticoids however with a high rate of recurrence after treatment discontinuation.

[Biologics in asthma: what's new?]. / Allergologie--immunologie clinique. (2.) Les biologiques dans l'asthme: quoi de neuf?

Biologic therapies such as monoclonal antibodies are currently being developed in the field of asthma. The molecules mentioned in this article, for the majority still under development, are expected to treat certain severe asthma subgroups in a more optimal way in the near future.

[Food allergy or food intolerance?]. / Allergie ou intolérance alimentaire?

Adverse food reactions can be classified into two main categories depending on wether an immune mechanism is involved or not. The first category includes immune mediated reactions like IgE mediated food allergy, eosinophilic oesophagitis, food protein-induced enterocolitis syndrome and celiac disease. The second category implies non-immune mediated adverse food reactions, also called food intolerances. Intoxications, pharmacologic reactions, metabolic reactions, physiologic, psychologic or reactions with an unknown mechanism belong to this category. We present a classification of adverse food reactions based on the pathophysiologic mechanism that can be useful for both diagnostic approach and management.

Two cases of interferon-alpha-induced sarcoidosis Koebnerized along venous drainage lines: new pathogenic insights and review of the literature of interferon-induced sarcoidosis.

Sarcoidosis is a systemic granulomatous disorder of unknown origin commonly affecting the lung, the lymphoid system and the skin. We report here two cases of cutaneous sarcoidosis in two former intravenous drug users following interferon (IFN)-α and ribavirin therapy for chronic hepatitis C. Both patients developed skin sarcoidosis along venous drainage lines of both forearms, coinciding with the areas of prior drug injections. The unique distribution of the skin lesions suggests that tissue damage induced by repeated percutaneous drug injections represents a trigger for the local skin manifestation of sarcoidosis. Interestingly, skin damage was recently found to induce the local expression IFN-α, a well-known trigger of sarcoidosis in predisposed individuals. Here we review the literature on sarcoidosis elicited in the context of IFN-α therapy and propose a new link between the endogenous expression of IFN-α and the induction of disease manifestations in injured skin.

[Common variable immune deficiency: what you need to know]. / Immunodéficience commune variable: ce qu'il faut savoir.

Common variable immune deficiency is the most frequent primary immune deficiency, characterized mainly by a disorder of B lymphocytes differentiation and a deficit in immunoglobulins. The clinical manifestations include recurrent infections, non-infectious lung and digestive involvements, autoimmune diseases, and an increased susceptibility to cancers. Recent breakthroughs have been made in the understanding of some genetic mechanisms of the disease. Replacement therapy with intravenous immunoglobulins remains the treatment of choice, which allows significant improvement in the survival and quality of life. However progress should be made in the understanding of the pathophysiology and in the early detection of this disease, since a delay in the diagnosis may have harmful consequences in terms of morbidity and mortality.

Genetics of resistance to two strains of soybean mosaic virus in differential soybean genotypes.

There are seven pathotypes of soybean mosaic virus (SMV) representing seven strain groups (G1-G7) in the United States. Soybean genotypes [Glycine max (L.) Merr.] may exhibit resistant (R), susceptible (S), or necrotic (N) reactions upon interacting with different SMV strains. This research was conducted to investigate whether reactions to two SMV strains are controlled by the same gene or by separate genes. Two SMV-resistant soybean lines, LR1 and LR2, were crossed with the susceptible cultivar Lee 68. LR1 contains a resistance gene Rsv1-s and is resistant to strains G1-G4 and G7. LR2 contains the Rsv4 gene and is resistant to strains G1-G7. Two hundred F(2:3) lines from LR1 x Lee 68 and 262 F(2:3) lines from LR2 x Lee 68 were screened for SMV reaction. Seeds from each F2 plant were randomly divided into two subsamples. A minimum of 20 seeds from each subsample were planted in the greenhouse and plants were inoculated with either G1 or G7. G1 is the least virulent, whereas G7 is the most virulent strain of SMV. The results showed that all the F(2:3) lines from both crosses exhibited the same reaction to G1 and G7. No recombinants were found in all the progenies for reactions to G1 and G7 in either cross. The results indicate that reactions to both G1 and G7 are controlled by either the same gene or very closely linked genes. This research finding is valuable for studying the resistance mechanism and interactions of soybean genotypes and SMV strains and for breeding SMV resistance to multiple strains.

Recombination within a nucleotide-binding-site/leucine-rich-repeat gene cluster produces new variants conditioning resistance to soybean mosaic virus in soybeans.

The soybean Rsv1 gene for resistance to soybean mosaic virus (SMV; Potyvirus) has previously been described as a single-locus multi-allelic gene mapping to molecular linkage group (MLG) F. Various Rsv1 alleles condition different responses to the seven (G1-G7) described strains of SMV, including extreme resistance, localized and systemic necrosis, and mosaic symptoms. We describe the cloning of a cluster of NBS-LRR resistance gene candidates from MLG F of the virus-resistant soybean line PI96983 and demonstrate that multiple genes within this cluster interact to condition unique responses to SMV strains. In addition to cloning 3gG2, a strong candidate for the major Rsv1 resistance gene from PI96983, we describe various unique resistant and necrotic reactions coincident with the presence or absence of other members of this gene cluster. Responses of recombinant lines from a high-resolution mapping population of PI96983 (resistant) x Lee 68 (susceptible) demonstrate that more than one gene in this region of the PI96983 chromosome conditions resistance and/or necrosis to SMV. In addition, the soybean cultivars Marshall and Ogden, which carry other previously described Rsv1 alleles, are shown to possess the 3gG2 gene in a NBS-LRR gene cluster background distinct from PI96983. These observations suggest that two or more related non-TIR-NBS-LRR gene products are likely involved in the allelic response of several Rsv1-containing lines to SMV.

Genetic study of a lethal necrosis to soybean mosaic virus in PI 507389 soybean.

PI 507389 soybean [Glycine max (L.) Merr.], a large-seeded line from Japan, exhibits a rapid, lethal, necrotic response to strains G1, G2, G5, and G6 of soybean mosaic virus (SMV). Unlike the hypersensitive necrotic reaction, this stem-tip necrosis can be a serious threat to soybean production. To investigate the genetic basis of lethal necrosis (LN), PI 507389 was crossed with the susceptible (S) cv. Lee 68 and with resistant (R) lines PI 96983, cv. York, and cv. Marshall, which carry single dominant genes for SMV resistance at the Rsv1 locus. F(1) plants, F(2) populations, and F(2:3) lines were inoculated with G1 and G6 in the greenhouse or in the field. Results indicated that LN is controlled by a single gene allelic to Rsv1, and this allele in PI 507389 is recessive to R alleles in PI 96983, York, and Marshall. The LN allele is codominant with the allele for S, for the heterozygotes showed a mixed phenotype of both necrosis (N) and mosaic (M) symptoms (NM). The LN allele becomes recessive to the S allele as the mixed NM shifts to S at a later stage in response to more virulent strains. The gene symbol Rsv1-n is assigned for the allele conferring LN in PI 507389. Rsv1-n is the only allele at the Rsv1 locus conditioning N to G1 and no R to any other SMV strains, and thus a unique genotype for SMV strain differentiation. The phenotypic expression of heterozygotes and the dominance relationships among R, N, and S depend on the virulence of SMV strains, source of alleles, and developmental stage.

Complementary action of two independent dominant genes in Columbia soybean for resistance to Soybean mosaic virus.

A stem-tip necrosis disease was observed in the soybean [Glycine max (L.) Merr.] cultivar Columbia and its derivative OX686 when infected with a necrosis-causing strain of Soybean mosaic virus (SMV) in Canada. A dominant gene named Rsv3 was found in OX686 for the necrotic reaction. In the present research we have found that Columbia is resistant to all known SMV strains G1-G7, except G4. Genetic studies were conducted to investigate the inheritance of resistance in Columbia and interactions of resistance gene(s) with SMV strains. Columbia was crossed with a susceptible cultivar, Lee 68, and with resistant lines PI96983, Ogden, and LR1, each possessing a resistance gene at the Rsv1 locus. F(1) individuals, F(2) populations, and F(2:3) lines from these crosses were inoculated with G7 or G1 in the greenhouse. Our inheritance data confirmed the presence of two independent dominant genes for SMV resistance in Columbia. Results from allelism tests further demonstrate that the two genes (referred to as R3 and R4 in this article) in Columbia were independent of the Rsv1 locus. R3 appears to be the same gene previously reported as Rsv3 in OX686, which was derived from Columbia. The R3 gene confers resistance to G7, but necrosis to G1. The other gene, R4, conditions resistance to G1 and G7 at the early seedling stage and then a delayed mild mosaic reaction (late susceptible) 3 weeks later. Plants carrying both the R3 and R4 genes were completely resistant to both G1 and G7, indicating that the two genes interact in a complementary fashion. Plants heterozygous for R3 or R4 exhibited systemic necrosis or late susceptibility, suggesting that the resistance is allele dosage dependent. The R4 gene appeared epistatic to R3 since it masked expression of necrosis associated with the response of R3. The complementary interaction of two resistance genes, as exhibited in Columbia, can be useful in development of soybean cultivars with multiple and durable resistance to SMV.

Mapping tightly linked genes controlling potyvirus infection at the Rsv1 and Rpv1 region in soybean.

Soybean mosaic virus (SMV) and peanut mottle virus (PMV) are two potyviruses that cause yield losses and reduce seed quality in infested soybean (Glycine max (L.) Merr.) fields throughout the world. Rsv1 and Rpv1 are genes that provide soybean with resistance to SMV and PMV, respectively. Isolating and characterizing Rsv1 and Rpv1 are instrumental in providing insight into the molecular mechanism of potyvirus recognition in soybean. A population of 1056 F2 individuals from a cross between SMV- and PMV-resistant line PI 96983 (Rsv1 and Rpv1) and the susceptible cultivar 'Lee 68' (rsv1 and rpv1) was used in this study. Disease reaction and molecular-marker data were collected to determine the linkage relationship between Rsv1, Rpv1, and markers that target candidate disease-resistance genes. F2 lines showing a recombination between two of three Rsv1-flanking microsatellite markers were selected for fine mapping. Over 20 RFLP, RAPD, and microsatellite markers were used to map 38 loci at high-resolution to a 6.8-cM region around Rsv1 and Rpv1. This study demonstrates that Rsv1 and Rpv1 are tightly linked at a distance of 1.1 cM. In addition, resistance-gene candidate sequences were mapped to positions flanking and cosegregating with these resistance loci. Based on comparisons of genetic markers and disease reactions, it appears likely that several tightly linked genes are conditioning a resistance response to SMV. We discuss the specifics of these findings and investigate the utility of two disease resistance related probes for the screening of SMV or PMV resistance in soybean.

Characterization of SMV Resistance Genes in Tousan 140 and Hourei Soybean.

'Tousan 140' and 'Hourei', two soybean [Glycine max (L) Merr.] accessions from Japan, each possess a single gene at different loci for resistance to Japanese Soybean mosaic virus (SMV) strain SMV C. However, more genetic information is needed to utilize these lines in a breeding program. The objectives of this study were to determine (i) the reaction of Tousan 140 and Hourei to SMV-G1 through G7 strains, (ii) the inheritance of SMV resistance in Tousan 140 and Hourei to strains SMV-G1 and G7, and (iii) the allelomorphic relationship of resistance genes in these accessions with previously known resistance genes. Tousan 140 and Hourei were crossed with SMV susceptible cultivar Lee 68 to study the inheritance of resistance. They were also crossed with lines possessing Rsv1, Rsv3, and putative Rsv4, and to each other, to elucidate the allelomorphic relationships among the genes in Tousan 140, Hourei, and previously reported genes. Inheritance and allelism studies indicated that Tousan 140 possesses two SMV resistance genes. These two genes were separated in two F(2:3) lines. One of the genes, an allele of Rsv1, expresses resistance to SMV-G1 through G3 and susceptibility to SMV-G5 through G7 while the other one, an allele of Rsv3, expresses resistance to SMV-G5 through G7 and susceptibility to SMV-G1 through G3. Their presence in Tousan 140 makes it resistant to strains SMV-G1 through G7. Hourei also is resistant to SMV-G1 through G7 and possesses two SMV resistance genes, which are also alleles of Rsv1 and Rsv3. One, probably the Rsv1 allele, expresses resistance to SMV-G1 and G7 and the other, probably the Rsv3 allele, expresses resistance to SMV-G7, but is susceptible to G1.

Genetic and Sequence Analysis of Markers Tightly Linked to the Soybean mosaic virus Resistance Gene, Rsv3.

Soybean mosaic virus (SMV) is a major viral pathogen, affecting soybean [Glycine max (L.) Merr.] production worldwide. The Rsv3 gene of soybean confers resistance to three of the most virulent strains (G5-G7) of SMV. The objectives of this study were to map Rsv3 and develop polymerase chain reaction (PCR) based markers for marker-assisted selection (MAS) purposes. Disease-response data were collected from two F(2) mapping populations, L29 (Rsv3) x Lee68 (rsv3) and Tousan 140 (Rsv3) x Lee68 (rsv3). Bulk segregant analysis based on amplified fragment length polymorphism (AFLP) markers demonstrated that the Rsv3 locus maps to the soybean molecular linkage group (MLG) B2 between restriction fragment length polymorphism (RFLP) markers A519 and Mng247. These two tightly linked RFLP markers were converted to PCR-based markers to expedite MAS. Sequence analysis of the Mng247 genomic region revealed similarity to the consensus sequence of a leucine-rich repeat (LRR) characteristic of the extracellular LRR class of disease resistance genes. Results from this study will be useful in pyramiding viral resistance genes and in cloning the Rsv3 gene.

Inheritance and allelism of resistance to soybean mosaic virus in Zao18 soybean from China.

Soybean mosaic disease caused by soybean mosaic virus (SMV) occurs wherever soybean [Glycine max (L.) Merr.] is grown and is considered one of the most important soybean diseases in many areas of the world. Use of soybean cultivars with resistance to SMV is a very effective way of controlling the disease. China has rich soybean germplasm, but there is very limited information on genetics of SMV resistance in Chinese soybean germplasm and reaction of the resistance genes to SMV strains G1-G7. There also is no report on allelic relationships of resistance genes in Chinese soybeans with other named genes at the three identified loci Rsv1, Rsv3, and Rsv4. The objectives of this study were to examine reactions of Chinese soybean cultivar Zao18 to SMV strains G1-G3 and G5-G7, to reveal the inheritance of SMV resistance in Zao18 and to determine the allelic relationship of resistance genes in Zao18 with previously reported resistance genes. Zao18 was crossed with the SMV-susceptible cultivar Lee 68 to study the inheritance of resistance. Zao18 was also crossed with the resistant lines PI96983, L29, and V94-5152, which possess Rsv1, Rsv3, and Rsv4, respectively, to examine the allelic relationship between the genes in Zao18 and genes at these three loci. Our research results indicated that Zao18 possesses two independent dominant genes for SMV resistance, one of which is allelic to the Rsv3 locus; the other is allelic with Rsv1. The presence of both genes (Rsv1 and Rsv3) in Zao18 confers resistance to SMV strains G1-G7.

Inheritance and allelism tests of Raiden soybean for resistance to soybean mosaic virus.

The gene symbol Rsv2 was previously assigned to the gene in the soybean [Glycine max (L.) Merr.] line OX670 for resistance to soybean mosaic virus (SMV). The Rsv2 gene was reported to be derived from the Raiden soybean (PI 360844) and to be independent of Rsv1. Accumulated data from our genetic experiments were in disagreement with this conclusion. In this study, Raiden and L88-8431, a Williams BC5 isoline with SMV resistance derived from Raiden, were crossed with two SMV-susceptible cultivars to investigate the mode of inheritance of SMV resistance in Raiden. They were also crossed with five resistant cultivars to examine the allelomorphic relationships of the Raiden gene with other reported genes at the Rsv1 locus. F1 plants, F2 populations, and F2-derived F3 (F2:3) lines were tested with SMV strains G1 or G7 in the greenhouse or in the field. The individual plant reactions were classified as resistant (R, symptomless), necrotic (N, systemic necrosis), or susceptible (S, mosaic). The F2 populations from R x S crosses segregated in a ratio of 3 (R + N):1 S and the F2:3 lines from Lee 68 (S) x Raiden (R) exhibited a segregation pattern of 1 (all R):2 segregating:1 (all S). The F2 populations and F2:3 progenies from all R x R crosses did not show any segregation for susceptibility. These results demonstrate that the resistance to SMV in Raiden and L88-8431 is controlled by a single dominant gene and the gene is allelic to Rsv1. The heterozygous plants from R x S and R x N crosses exhibited systemic necrosis when inoculated with SMV G7, indicating a partial dominance nature of the resistance gene. Raiden and L88-8431 are both resistant to SMV G1-G4 and G7, but necrotic to G5, G6, and G7A. Since the resistance gene in Raiden is clearly an allele at the Rsv1 locus and it exhibits a unique reaction to the SMV strain groups, assignment of a new gene symbol, Rsv1-r, to replace Rsv2 would seem appropriate. Further research is ongoing to investigate the possible existence of the Rsv2 locus in OX670 and its relatives.

In vitro investigations with the histamine H1 receptor antagonist, epinastine (WAL 801 CL), on isolated human allergic effector cells.

OBJECTIVE AND DESIGN: Skin mast cells, basophils and eosinophils are effector cells of acute and subacute allergic responses due to their capacity to produce a large number of (pro)inflammatory mediators. Histamine H1 receptor antagonists, such as epinastine (WAL 801 CL), have been described to partially exert antiallergic and antiinflammatory effects both in vivo and in vitro in addition to their antihistaminergic properties. The aim of the present study was to investigate whether epinastine could influence the in vitro activation of isolated human skin mast cells, basophils and eosinophils induced by different secretagogues. METHODS: Cells were isolated from healthy women following plastic surgery and healthy blood donors, respectively. Mast cells were isolated by enzymatic digestion of the skin. Blood cells were isolated by gradient centrifugation and negative selection with magnetic beads. RESULTS: A wide range of concentrations of the drug (1 nmol/l to 100 micromol/l) did not significantly inhibit histamine release from basophils induced by immunologic (anti-IgE, concanavalin A, priming factors interleukin-3 and interleukin-5) and non immunologic (A23187, ionomycin, 12-o-tetradecanoyl-phorbol-13-acetate, C5a, formyl-methionyl-leucyl-phenylalanine) stimuli. Furthermore, the drug had no effect on A23187-induced release of eosinophil cationic protein from eosinophils. However, at a concentration >0.1 nmol/l, IgE-mediated LTC4 production from basophils was significantly suppressed. Histamine release from skin mast cells due to anti-IgE or A23187 was inhibited by epinastine in a dose-dependent fashion, whereas substance P-induced activation as well as stem cell factor priming were not. Epinastine did not inhibit isolated protein kinase C from rat brain. CONCLUSION: The results confirm previous in vivo and in vitro observations obtained from animal models that epinastine exerts antiallergic and antiinflammatory effects. Whether the observed effects are due to non specific membrane interactions or by influencing intracellular signal transduction elements has to be further elucidated.

Isolation of a superfamily of candidate disease-resistance genes in soybean based on a conserved nucleotide-binding site.

The tobacco N and Arabidopsis RPS2 genes, among several recently cloned disease-resistance genes, share highly conserved structure, a nucleotide-binding site (NBS). Using degenerate oligonucleotide primers for the NBS region of N and RPS2, we have amplified and cloned the NBS sequences from soybean. Each of these PCR-derived NBS clones detected low-or moderate-copy soybean DNA sequences and belongs to 1 of 11 different classes. Sequence analysis showed that all PCR clones encode three motifs (P-loop, kinase-2, and kinase-3a) of NBS nearly identical to those in N and RPS2. The intervening region between P-loop and kinase-3a of the 11 classes has high (26% average) amino acid sequence similarity to the N gene although not as high (19% average) to RPS2. These 11 classes represent a superfamily of NBS-containing soybean genes that are homologous to N and RPS2. Each class or subfamily was assessed for its positional association with known soybean disease-resistance genes through near-isogenic line assays, followed by linkage analysis in F2 populations using restriction fragment length polymorphisms. Five of the 11 subfamilies have thus far been mapped to the vicinity of known soybean genes for resistance to potyviruses (Rsv1 and Rpv), Phytophthora root rot (Rps1, Rps2, and Rps3), and powdery mildew (rmd). The conserved N- or RPS2-homologous NBS sequences and their positional associations with mapped soybean-resistance genes suggest that a number of the soybean disease-resistance genes may belong to this superfamily. The candidate subfamilies of NBS-containing genes identified by genetic mapping should greatly facilitate the molecular cloning of disease-resistance genes.

Amplified fragment length polymorphism (AFLP) in soybean: species diversity, inheritance, and near-isogenic line analysis.

Amplified fragment length polymorphism (AFLP) analysis is a PCR-based technique capable of detecting more than 50 independent loci in a single PCR reaction. The objectives of the present study were to: (1) assess the extent of AFLP variation in cultivated (Gycine max L. Merr.) and wild soybean (G. soja Siebold & Zucc.), (2) determine genetic relationships among soybean accessions using AFLP data, and (3) evaluate the usefulness of AFLPs as genetic markers. Fifteen AFLP primer pairs detected a total of 759 AFLP fragments in a sample of 23 accessions of wild and cultivated soybean, with an average of 51 fragments produced per primer pair per accession. Two-hundred and seventy four fragments (36% of the total observed) were polymorphic, among which 127 (17%) were polymorphic in G. max and 237 (31%) were polymorphic in G. soja. F2 segregation analysis of six AFLP fragments indicated that they segregate as stable Mendelian loci. The number of polymorphic loci detected per AFLP primer pair in a sample of 23 accessions ranged from 9 to 27. The AFLP phenotypic diversity values were greater in wild than in cultivated soybean. Cluster and principal component analyses using AFLP data clearly separated G. max and G. soja accessions. Within the G. max group, adapted soybean cultivars were tightly clustered, illustrating the relatively low genetic diversity present in cultivated soybean. AFLP analysis of four soybean near-isogenic lines (NILs) identified three AFLP markers putatively linked to a virus resistance gene from two sources. The capacity of AFLP analysis to detect thousands of independent genetic loci with minimal cost and time requirements makes them an ideal marker for a wide array of genetic investigations.

Molecular-marker analysis of seed-weight: genomic locations, gene action, and evidence for orthologous evolution among three legume species.

The objectives of this study were to use molecular markers to: (1) identify quantitative trait loci (QTL) controlling seed-weight in soybean, (2) characterize the genetic basis of seed-weight expression, and (3) determine whether soybean shares orthologous seed-weight genes with cowpea and/or mung bean. An F2 population was developed between a large-seeded Glycine max breeding line and a small-seeded G. soja plant introduction. DNA samples from 150 F2 individuals were analyzed with 91 polymorphic genetic markers, including RFLPs, RAPDs and SSRs. Seed-weight was analyzed by randomly sampling 100 seeds from each of 150 greenhouse-grown F2 individuals, and their 150 F2∶3 lines, from a replicated field trial. Markers associated with seed-weight were identified using the computer program MapMaker-QTL and a one-way analysis of variance. Three and five markers were significantly associated with seed-weight variation (P<0.01) in the F2 and F2∶3 generations, respectively. Tests for digenic epistasis revealed three significant interactions in both generations. In a combined analysis, these markers and interactions explained 50 and 60% of the phenotypic variation for seed-weight in the F2 and F2∶3 generations, respectively. Comparison of our results in soybean (Glycine) with those previously reported in cowpea and mung bean (Vigna) indicated that soybean and cowpea share an orthologous seed-weight gene. In both species, a genomic region significantly associated with seed-weight spanned the same RFLP markers in the same linkage order. A significant digenic interaction involving this genomic region was conserved in all three species. These results suggest that the exploitation of "comparative QTL mapping" is an invaluable tool for quantitative geneticists working with poorly characterized plant systems.