From Mendel’s discovery on pea to today’s plant genetics and breeding

In 2015, we celebrated the 150th anniversary of the presentation of the seminal work of Gregor Johann Mendel. While Darwin’s theory of evolution was based on differential survival and differential reproductive success, Mendel’s theory of heredity relies on equality and stability throughout all stages of the life cycle. Darwin’s concepts were continuous variation and “soft” heredity; Mendel espoused discontinuous variation and “hard” heredity. Thus, the combination of Mendelian genetics with Darwin’s theory of natural selection was the process that resulted in the modern synthesis of evolutionary biology. Although biology, genetics, and genomics have been revolutionized in recent years, modern genetics will forever rely on simple principles founded on pea breeding using seven single gene characters. Purposeful use of mutants to study gene function is one of the essential tools of modern genetics. Today, over 100 plant species genomes have been sequenced. Mapping populations and their use in segregation of molecular markers and marker–trait association to map and isolate genes, were developed on the basis of Mendel's work. Genome-wide or genomic selection is a recent approach for the development of improved breeding lines. The analysis of complex traits has been enhanced by high-throughput phenotyping and developments in statistical and modeling methods for the analysis of phenotypic data. Introgression of novel alleles from landraces and wild relatives widens genetic diversity and improves traits; transgenic methodologies allow for the introduction of novel genes from diverse sources, and gene editing approaches offer possibilities to manipulate gene in a precise manner

‘Forrest’ Resistance to the Soybean Cyst Nematode Is Bigenic: Saturation Mapping of the Rhg1 and Rhg4 Loci

Field resistance to cyst nematode (SCN) race 3 (Heterodera glycines I.) in soybean [Glycine max (L.) Merr.] cv ‘Forrest’ is conditioned by two QTLs: the underlying genes are presumed to include Rhg1 on linkage group G and Rhg4 on linkage group A2. A population of recombinant inbred lines (RILs) and two populations of near-isogenic lines (NILs) derived from a cross of Forrest × Essex were used to map the loci affecting resistance to SCN. Bulked segregant analysis, with 512 AFLP primer combinations and microsatellite markers, produced a high-density genetic map for the intervals carrying Rhg1 and Rhg4. The two QTLs involved in resistance to SCN were strongly associated with the AFLP marker EATGMCGA87 (P = 0.0001, R2 = 24.5%) on linkage group G, and the AFLP marker ECCGMAAC405 (P = 0.0001, R2 = 26.2%) on linkage group A2. Two-way analysis of variance showed epistasic interaction (P = 0.0001, R2 =16%) between the two loci controlling SCN resistance in Essex × Forrest recombinant inbred lines. Considering the two loci as qualitative genes and the resistance as female index FI \u3c 5%, jointly the two loci explained over 98% of the resistance. The locations of the two QTLs were confirmed in the NILs populations. Therefore SCN resistance in Forrest × Essex is bigenic. High-efficiency marker-assisted selection can be performed using the markers to develop cultivars with stable resistance to SCN