Nowadays Charles Darwin is recognised as the scientist most associated with the theory of
evolution but there were others whose ideas were later shunned. Darwin's theory of evolution had
three main concepts. First, that variation occurred randomly among members of a species;
second that an individual trait could be inherited and lastly that the struggle for existence would
allow only those with favourable traits to survive. New evidence is revealing that life
is not this simple and that some of the older ideas also seem to have equal merit
in trying to understand the process. Let's dive in and find out more...
Jean-Baptiste Lamarck was a French scientist
who developed an alternative theory before Charles Darwin.
Overall Lamarck's concept was limited in scope. He did not believe in the extinction
of species but rather thought that species are gradually transformed into other species.
He viewed that organisms had an innate tendency to progress towards perfection
down the succession of generations.
There were two important concepts in this model.
1. A characteristic which is used more and more by an organism
becomes bigger and stronger, and one that is not used eventually
disappears. This would later be called Inheritance of acquired characteristics.
2. Any feature of an organism that is improved through use is passed to its offspring
Darwin was well aware of Lamarck's work and generously acknowledged his contribution. His view
of the inheritance of acquired characteristics dramatically evolved over his lifetime.
Initially, he felt it was only a very small component but in later publications,
he viewed it as being more consequentially. Even in Darwin's day, many scientists considered his
giving into Larmarckian inheritance a sign of weakness and a mistake.
Over the centuries the idea of Lamarckian inheritance became repulsive
and unacceptable to most biologists. It is viewed as a derogatory phrase
and is presented as a grave error in judgement.
However, biologists are finding more and more examples
of evolution scenarios that seem to blur the line between both concepts.
Before we look at some examples it is important to define the Lamarckian paradigm
and the criteria an evolutionary process must satisfy to be considered Lamarckian.
At its most basic level, we can describe the causal chain as ENVIRONMENT - HABIT - FORM.
Lamarck stated the following: "Whatever the environment may do, it does not
work any direct modification whatever in the shape and organization of animals. But great alterations
in the environment of animals lead to great alterations in their needs, and these alterations
in their needs necessarily lead to others in their activities. Now if the new needs become permanent,
the animals then adopt new habits that last as long as the needs that evoked them"
So we could state the Lamarck scheme as follows:
1. Environmental factors cause genomic changes
2. the induced changes are targeted to a specific gene
3. the induced changes provide adaptation to the original causative factor
By comparison, Darwin's route of evolution is that the environment is not the causative agency
but merely a selective force that may promote the fixation of random changes that may
cause adaptation. In this sense the Darwinian scheme is simpler and less demanding compared
to the Lamarckian one in that no specialised mechanisms are required to direct the change
to the relevant genome, restrict it to a specific mutation to provide the relevant adaptation.
It is this complexity that makes conceiving and finding this mechanism of direct adaptation in
genomes so difficult and has relegated it to a crackpot idea simply to be ignored.
1. Antivirus immunity in prokaryotes
A recently discovered novel system of antiphage defence in archaea and bacteria seems to function
via a straightforward Lamarckian mechanism. The system is known as CRISPR-Cas, where CRISPR
stands for Clustered Regularly Interspaces Short Palindromic Repeats and CAS for CRISPR associated
genes. CRISPR is a way of finding a specific bit of DNA inside a cell and then editing it.
CRISPR have been known about for over 20 years, even before the first bacterial
genome was sequenced. It was discovered that some of the inserts in CRISPR cassettes
are identical to fragments of bacteriophage. This led to the idea that CRISPR-Cas system
utilised the phage derived sequences as guide molecules to destroy phage mRNA.
This is a Lamarckian system - an environmental cue is
employed to directly modify the genome - the resulting modification directly affects
the same cue that caused the modification - the modification is clearly adaptive
and is inherited by the offspring of the cell that encountered the mobile element
2. Horizontal gene transfer
Prokaryotes readily obtain DNA from the environment.
The absorbed DNA often integrates into prokaryotic chromosomes and can be fixed in a population if
the transferred genetic material confers even a slight selective advantage onto the recipient.
The process of horizontal gene transfer has obvious Lamarckian aspects to it. DNA
is acquired from the environment, and if it infers an adaptive value is passed on.
A prime example of this behaviour is the evolution of antibiotic resistance.
When a sensitive prokaryote enters an environment where an antibiotic is present, the only chance
for the newcomer to survive is to acquire a resistance gene through horizontal gene transfer.
This typically occurs via a plasmid and is a clear case of Lamarckian inheritance.
Recent comparative genomic studies indicate that horizontal gene transfer
is the principal mode of bacterial adaptation to the environment through the extension of
metabolic and signalling networks that integrate newly acquired genes and thereby incorporate new
capabilities within pre-existing frameworks. Quantitatively, in prokaryotes, Horizontal gene
transfer appears to be a far more important route of adaptation than gene duplication.
3. Stress-induced mutagenesis and activation of mobile elements
In the classical experiment, McClintock demonstrated activation of 'gene jumping'
in plants under stress and the importance of this stress-induced
mobility of distinct 'controlling elements' for the emergence of resistance phenotypes.
An example of this is the mutagenic SOS repair pathways in E. coli. The adaptive character
of error-prone DNA repair is supported by several strong lines of evidence. Mutations
produced by error-prone repair processes, although not targeted to specific genes,
are not randomly scattered in the genome either. They seem to cluster in functionally linked
genes where beneficial mutations emerge while limiting the damage to other parts of the genome.
Stress-induced mutagenesis is a rule among bacteria rather than an exception.
Although this type of mechanism is not exactly Lamarckian. As the stress does not
cause mutations directly and specifically in genes conferring stress resistance.
Instead, the organisms evolved mechanisms that in response to stress
induce non-specific mutagenesis which seems to be fine-tuned so that it minimises the
damage from the alterations in those rare genomes that carry a beneficial mutation.
This type of mechanism is triggered by environmental conditions. This leads to mutations
which are adaptations to the stress factor. So in simple terms if the environment changes which
in turn causes stress to the bacteria, like a shortage of food or exposure to something harmful.
The stress causes mutations in the bacteria which can lead to the evolution of mutations
which can help it overcome the stress factor. These are then passed on to its offspring.
4. Non-random mutations in humans
A new study has brought the first evidence of nonrandom mutations in human genes,
challenging a core assumption at the heart of evolutionary theory
by showing a long-term directional mutational response to environmental pressure.
The team developed a method for identifying mutations that would arise out of the blue
in their offspring without being inherited from either parent. They used this to examine the out
of the blue emergence of the human haemoglobin S mutation, which is probably the most well-known
point mutation in biology. This mutation provides protection against malaria for people with
one copy but causes sickly-cell anaemia in those with two. Malaria has arguably been the strongest
selection pressure acting on humans in the last 10,000 years. It often causes more than
a million deaths per year in Africa in the recent past. It is often used as an example of random
mutation and natural selection in evolution. The assumption being that is arose accidentally in
an individual in sub-Saharan Africa and then spread inside Africa via natural selection
until its malaria-protective benefits were balanced out by its sickle-cell anaemia costs.
By examining the out of the blue origination of the mutation,
the scientists were able to disentangle whether the malaria protective mutation arises randomly
and spread in Africa only because of selection pressure or instead whether it could actually
be occurring out of the blue more often in sub-Saharan Africans who have been exposed
to intense malarian selection pressure for many generations. If the mutation is random then it
should be equally likely to emerge in areas of high malaria versus areas of low malaria.
The results of their analysis clearly demonstrated that the mutations exhibited a non-random pattern.
The mutations appeared out of the blue not only much faster than expected
but also much faster in the population where it is of adaptive significance.
These mutations all go to demonstrate that we need to move away from our
traditional thinking on the topic. Neither Darwin nor Lamarck are entirely correct.
The systems are far more complex and there seems to be an interplay
between information that is stored in the genome and the environmental pressures.