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The two forms of genetic drift are the bottleneck effect and the founder effect.


Genetic drift is an unpredictable change in the gene pool, and it usually limits diversity because some alleles become either eliminated or expressed too much.

Two forms of genetic drift are the founder effect and the bottleneck effect.

1. Founder effect

When a small group of individuals breaks away from a larger population and creates its own population in a separate location, rare alleles could be overrepresated in this newly "founded" population. If this new population is isolated and interbreeds, then the resulting population could have a high frequency of certain traits.

Example: The Afrikaner (Dutch) population that settled in South Africa had an abnormally high count of Huntington's Disease, because the first Dutch settlers had a high frequency of the gene (compared to the original Dutch population).

AP Biology Wiki

2. Bottleneck effect

The bottleneck effect occurs when a random event, such as a natural disaster, unselectively reduces the size of a population. The resulting population is much less genetically diverse than the original population. Some alleles may become entirely eliminated and some may become overrepresented .

Example: After the northern elephant seal almost went extinct as a result of extensive hunting, the seal was placed under government protection. Since then, the population has grown, but all the descendants have little genetic variation since so few elephant seals remained.



Nature selects the traits that give an organism an advantage over others. These traits are found in many other organisms. What they evolved from differs, but their mutations remain the same/similar.


There are two factors that allows an organisms to evolve and live. They are:

  1. Random mutations.
  2. The role of the environment.

The first factor, random mutations, have no specific role in answering your question. What matters is the second factor.

Now, as we all know, these mutations cannot help an organism unless there is some sort of requirement that ultimately leads to the organism gaining an advantage.

This is evident in all occasions. Normally, an organism will mutate and gain a certain trait. If this trait is beneficial, the organism will survive and pass this trait. Other organisms are susceptible to gaining this trait but nature selects for or against these traits for the organism.

This can be found (for example) between dolphins and sharks. They are very different from each other, but they all gain a certain characteristic that gives them an advantage over other animals (keep in mind these animals gain advantages over their predators).


A common characteristic in this case, would be a their stream-lined body for speed.


Like I said before, these animals are very different from each other, but they evolved to have similar characteristics in order to maximize efficiency when hunting. This is only one of the many examples of morphological interactions.

Hope this helps :)


Plants - cell wall forms.
Animals - cleavage furrow forms.


Cytokinesis occurs in mitosis and meiosis for both plant and animal cells. The ultimate objective is to divide the parent cell into daughter cells.

In plants , this occurs when a cell wall forms in between the daughter cells.



In animals , this occurs when a cleavage furrow forms. This pinches the cell in half.


Leaving Bio

Hope this helps :)


Lamarck's basic was alright: that evolutionary changes are inherent and there must be a mechanism. He inspired next generation biologists to propose alternative theories to explain the mechanism.


Lamarck's theory of inheritance of acquired characteristics theorized that an organism's responses to environmental stimuli (through use and disuse) would pass on to offspring as physical adaptations.

The most famous example of this was the long neck of African giraffe: Lamarck believed that giraffes had to stretch their necks to eat leaves on tall trees, hence they acquired bit longer necks in each generation and that, their offspring would be born with longer necks.

Of course, inheritance of acquired characters could not be proved to be true when German biologist August Weismann experimented by cutting tails of a number of white mice for successive generations. Moreover, a female bodybuilder will not necessarily give birth to an offspring with naturally huge muscles or for that matter, Chinese women never inherited small feet from their mothers.

But Lamarck didn't completely miss the mark either. He definitely understood that favorable traits passed into further generations and non-favorable traits receded, but just didn't understand how these traits appear in the gene pool.

We now know that these traits come through mutations, or errors in DNA replication, instead of repeated physical response to stimuli. Favourable mutations are simply conserved in the gene pool and hence with time genetic make up of population changes.

Lamarck developed a similar idea in 1809 when he concluded that a new species may eventually evolve from the existing species due to accumulation of new adaptive characters through generations.

This was a revolutionary concept in at least two ways:
One, he understood that environment has a role in shaping evolutionary history of organisms.
Two, he was the first biologist to confidently propose dynamicity of species concept (i.e. the species could change).

The above mentioned thoughts are integral part of later day evolutionary theories put forward by Wallace and Darwin.


There is a STOP code.


As we know after the transcription process, mRNA leaves the nucleus and attaches to ribosome small subunit in the cytoplasm.


The tRNA will carry an amino acid and its anticodon will bind to the complementary codon of mRNA: e.g. GUC (codon) will be bind to CAG (anticodon).


Refer to above table, we know the starting code for translation is AUG, for which the amino acid specified is methionine.

For the STOP codon we can have 3 probabilities which are UAA, UAG or UGA. There are no corresponding anticodon carrying tRNA for the stop codons. Hence no amino acid will get attached to the polypeptide chain when a stop codon gets exposed on the surface of ribosome.





This illustrations depicts the #color(magenta)"lock and key model"# of enzyme and substrate binding first proposed by Emile Fischer in his studies on enzymes in the nineteenth century.

#1."Shows the active sites of the enzyme."#
#2."Substrate complementary to the active sites of the enzyme."#
#3."Enzyme-substract complex forms."#
#4."Products released after catalyzed reaction."#
#5."Biological catalyst remains unchanged."#

The model proposes the idea that enzymes are like locks and substrates are the keys to that lock. The key has to match up perfectly to the grooves of lock, or in other words, be #color(magenta)"complementary"# to it.


This model, however, posed many problems to scientists because such an #color(magenta)"enzyme-substrate complex"# would lead to poor catalysis. The reason is after binding, the enzyme-substrate complex would become more stable than the substrate and thus it would be lower in free energy. And because it is lower in free energy, the #Delta"G"^"‡"("activation energy")#of the reaction would increase. Therefore, the #color(red)[Delta"G"^‡"catalyzed" >DeltaG^‡"uncatalyzed"#

enter image source here
In later studies, biochemists came up with a better model to explain how enzymes and substrates bind - #color(magenta)["the induced fit model"#.

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