Separate loci underlie resistance to root infection and leaf scorch during soybean sudden death syndrome

Soybean [Glycine max (L.) Merr.] cultivars show differences in their resistance to both the leaf scorch and root rot of sudden death syndrome (SDS). The syndrome is caused by root colonization by Fusarium virguliforme (ex. F. solani f. sp. glycines). Root susceptibility combined with reduced leaf scorch resistance has been associated with resistance to Heterodera glycines HG Type 1.3.6.7 (race 14) of the soybean cyst nematode (SCN). In contrast, the rhg1 locus underlying resistance to Hg Type 0 was found clustered with three loci for resistance to SDS leaf scorch and one for root infection. The aims of this study were to compare the inheritance of resistance to leaf scorch and root infection in a population that segregated for resistance to SCN and to identify the underlying quantitative trait loci (QTL). “Hartwig”, a cultivar partially resistant to SDS leaf scorch, F. virguliforme root infection and SCN HG Type 1.3.6.7 was crossed with the partially susceptible cultivar “Flyer”. Ninety-two F5-derived recombinant inbred lines and 144 markers were used for map development. Four QTL found in earlier studies were confirmed. One contributed resistance to leaf scorch on linkage group (LG) C2 (Satt277; P = 0.004, R 2 = 15%). Two on LG G underlay root infection at R8 (Satt038; P = 0.0001 R 2 = 28.1%; Satt115; P = 0.003, R 2 = 12.9%). The marker Satt038 was linked to rhg1 underlying resistance to SCN Hg Type 0. The fourth QTL was on LG D2 underlying resistance to root infection at R6 (Satt574; P = 0.001, R 2 = 10%). That QTL was in an interval previously associated with resistance to both SDS leaf scorch and SCN Hg Type 1.3.6.7. The QTL showed repulsion linkage with resistance to SCN that may explain the relative susceptibility to SDS of some SCN resistant cultivars. One additional QTL was discovered on LG G underlying resistance to SDS leaf scorch measured by disease index (Satt130; P = 0.003, R 2 = 13%). The loci and markers will provide tagged alleles with which to improve the breeding of cultivars combining resistances to SDS leaf scorch, root infection and SCN HG Type 1.3.6.7

Seasonal patterns of prolactin and corticosterone secretion in an Antarctic seabird that moults during reproduction

In avian species that have evolved life-history strategies wherein molt and breeding overlap, there are potential conflicts between the regulatory roles of baseline prolactin and corticosterone in parental care (positive) and moult (negative). We describe seasonal patterns of hormonal secretion, moult, and parental behaviour in sibling species of giant petrels (Macronectes spp.) which begin moult during the incubation/ early chick-rearing stage of reproduction. With the exception of male Southern giant petrels (Macronectes giganteus), prolactin secretion and moult in Northern (Macronectes halli) and female Southern giant petrels conformed to those observed in all other avian species, with the initiation of moult coincident with decreases from peak prolactin levels. However, male Southern giant petrels began moulting early in incubation when prolactin was increasing and had not yet peaked, which suggests a requirement of prolactin for incubation behaviour and a dissociation of prolactin from moult. Corticosterone showed little seasonal variation and no relationship with moult. When comparing prolactin, corticosterone, and moult in failed vs. active breeders, we found that failed breeding enabled a more rapid down-regulation of prolactin, thus facilitating a more rapid moult. We present specific examples of the behavioural ecology of giant petrels which we conclude help mediate any potential hormonal conflicts between parental care and moult