After two long centuries of evolutionary debate, it seems that we need to resurrect the ideas first put forward by Jean-Baptiste de Lamarck in 1809. The new genetics is providing us with extant evidence suggesting that nature has evolved a number of mechanisms to enable all organisms to evolve as they adapt to their environment: pondering the genesis of the epigenetic and mutational changes involved gives rise to a new theory of evolution based on the inheritance of acquired characters.

When Jean-Baptiste de Lamarck came up with the idea of acquired inheritance in 1809, he couldn't justify it [1]. However, the new genetics is providing us with molecular evidence suggesting that environmentally ‘directed' epigenetic changes, combined with targeted mutations best explains the new evolutionary model [2]. While some neo-Darwinians are still reluctant to accept a Lamarckian world view, many mainstream biologists are now openly supporting a Lamarckian view of evolution. But what mainstream scientific evidence is there to support the new theory of adaptive evolution?

Epigenetic Changes
The science of epigenetics is providing some of the most compelling evidence supporting the idea of acquired inheritance [3]. In the last decade we have discovered a number of molecular mechanisms that are used to write additional information onto the surface of our genes without altering the genomic sequence code. While some epigenetic mechanisms involve altering the surface of the individual nucleotides A, G, C or T/U, others involve changes in DNA folding patterns.
The main molecular mechanisms that mediate epigenetic regulation include DNA methylation and chromatin/histone modifications (see fig 1). Histone methylation plays a critical role in many epigenetic phenomena by producing conformational changes that switch genes to either an ‘off' state (not able to be transcribed), or an ‘on' state (able to be transcribed). These gene expression mechanisms enable the genome to rapidly adapt to a wide range of environmental changes, and they are responsible for generating diversity among individuals who may share the same DNA. Inheritance of this type of modification can occur rapidly to enable a species to adapt to sudden environmental change.

There are now a number of studies showing that what we eat, why birds suddenly build nests, the environmental stresses we are exposed to and even some subtle changes in behaviour by rat mothers can be inherited by first and subsequent generations of offspring.

One of the key questions raised by these findings is how was such a sophisticated ‘library' of genetic alternatives and cross-gene linkages created as we evolved? To answer this question, we need to evoke ways for environmental feedback to result in mutational changes in the genome.

Environmentally Directed Mutation
The inheritance of environmentally induced epigenetic change relies on a process for creating new genes or alternative gene associations in response to environmental stimuli at some stage in our evolutionary past. It implies that there are mechanisms for the creation and integration of new genomic information by generating environmentally directed mutations, and reverse transcription to integrate the favoured or selected changes into the genome (see fig 2). We now know that there are a range of environmentally directed mutations that are both time dependent and loci specific on the genome. While this view remains controversial among many scientists, there is now an expanding body of research suggesting that these processes are play an important role in generating adaptive mutations in a number of genes. A key step involves reverse transcription. The process can occur rapidly, or more slowly, and the changes can be inherited.

The antibody genes provide a wonderful example of how the genome is updated in response to an almost infinite variety of new foreign pathogens. The first clues that the antibody gene family might have developed as an adaptive process were provided through experiments conducted by Australian immunologist Ted Steele and his Canadian colleague Reg Gorczynski. To build a theoretical model to explain their predictions, Steele relied on Howard Temin's ideas on reverse transcription as the mechanism for new RNA to be integrated into the genomic DNA following exposure to a previously unknown pathogen. While it has taken almost three decades for Steele to be vindicated for proposing his Lamarckian model, we now know that the antibody genes are updated via a complex set of pathways involving targeted hypermutation and reverse transcription [4]. While some of the details of the somatic hypermutation mechanisms involved remain in dispute, the immune system provides a well studied model demonstrating how new pathogens in the environment have acted as the force guiding the evolution of the vertebrate antibody gene family.