For more than a century, modern genetics has been shaped by the pioneering work of Gregor Mendel, whose experiments with pea plants in the mid-19th century led to the foundational principles of inheritance still taught in biology classrooms today. But a new perspective published in the journal Genetics suggests that this classical view may no longer be sufficient to explain how biological traits are actually produced.

Axar.az reports that the authors of the study argue that while Mendelian genetics laid the groundwork for understanding heredity, it promotes an overly simplified model in which single genes determine single traits. Instead, they contend that most observable characteristics arise from complex interactions among thousands of genes, as well as environmental influences. This challenges the long-standing assumption that individual genes can be studied in isolation to fully explain biological variation.

The paper places this debate in a historical context, contrasting Mendel’s “particulate” model of inheritance with the biometric tradition associated with Francis Galton, which emphasized continuous variation such as height. According to the authors, modern quantitative genetics and genome-wide association studies (GWAS) have effectively revived and expanded this biometric perspective, showing that most traits are highly polygenic in nature.

Rather than being controlled by a small number of genes with large effects, complex traits are shaped by vast networks of genetic variants, each contributing a small portion of the overall phenotype. The authors argue that this reality limits the explanatory power of classical Mendelian approaches, particularly when studying variation across populations or attempting to understand complex diseases.

However, the researchers stop short of rejecting Mendelian genetics altogether. They acknowledge that it has been crucial for major advances in biology, including gene editing technologies and the identification of key genetic pathways. Still, they argue that it is insufficient on its own to explain why genomes produce such diverse outcomes across individuals.

The study also points to recent genomic findings that illustrate this complexity. For example, while researchers have now identified the seven loci originally studied by Mendel in peas, they have also found dozens of additional traits influenced by multiple genes acting together, reinforcing the idea that most biological traits are not purely single-gene driven.

The authors note that similar critiques have been raised before, including during the development of the Modern Synthesis in the early 20th century and more recently through GWAS research. Yet they argue that many areas of molecular biology remain anchored in a reductionist framework that prioritizes single-gene explanations.

In response, the paper calls for a shift toward experimental approaches that explicitly account for polygenicity. The authors suggest that future research should focus on large-scale genomic studies, environmental perturbations, and high-throughput phenotyping in order to better capture how genes interact to produce traits.

“Yet these attempts have failed to convince many molecular biologists who remain resistant to the idea that polygenicity can provide meaningful mechanistic insights,” the authors write. “We call once again for the community of researchers that engages in more classical genetics to also embrace the complexities of genotype–phenotype mapping.”

The study concludes that while Mendelian genetics remains a cornerstone of biology, understanding the full complexity of inheritance will require moving beyond single-gene thinking toward a more integrated, systems-level view of the genome.