DNA is in eachcell in the organism and tells cells whatproteins to make. Mostly, these proteins areenzymes. DNA isinherited by children from their parents. This is why children sharetraits with their parents, such as skin, hair and eye color. The DNA in a person is a combination of the DNA from each of their parents.
Part of an organism's DNA is "non-coding DNA" sequences. They do not code for protein sequences. Some noncoding DNA is transcribed intonon-coding RNA molecules, such astransfer RNA,ribosomal RNA, andregulatory RNAs.[2] Other sequences are not transcribed at all, or give rise to RNA of unknown function. The amount of non-coding DNA varies greatly among species. For example, over 98% of the human genome is non-coding DNA,[3] while only about 2% of a typicalbacterialgenome is non-coding DNA.
Insideeukaryotic cells, DNA is organized intochromosomes. Beforecell division, more chromosomes are made in the process ofDNA replication. Eukaryotic organisms like animals, plants, fungi and protists store most of their DNA inside thecell nucleus. But prokaryotes, like bacteria and archaea store their DNA only in thecytoplasm, in circular chromosomes. Inside eukaryotic chromosomes, chromatin proteins, such ashistones, help to compact and organize DNA.[5]
The 'rungs' of the DNA ladder are each made of two bases, one base coming from each leg. The bases connect in the middle: 'A'only pairs with 'T', and 'C'only pairs with 'G'. The bases are held together byhydrogen bonds.
Adenine (A) and thymine (T) can pair up because they make two hydrogen bonds, and cytosine (C) and guanine (G) pair up to make three hydrogen bonds. Although the bases are always in fixed pairs, the pairs can come in any order (A-T or T-A; similarly, C-G or G-C). This way, DNA can write 'codes' out of the 'letters' that are the bases. These codes contain the message that tells the cell what to do.
On chromosomes, the DNA is bound up withproteins calledhistones to formchromatin. This association takes part inepigenetics andgene regulation. Genes are switched on and off during development and cell activity, and this regulation is the basis of most of the activity which takes place in cells.
When DNA is copied, this is calledDNA replication. Briefly, the hydrogen bonds holding together paired bases are broken and the molecule is split in half: the legs of the ladder are separated. This gives two single strands. New strands are formed by matching the bases (A with T and G with C) to make the missing strands.
First, anenzyme called DNA helicase splits the DNA down the middle by breaking the hydrogen bonds. Then after the DNA molecule is in two separate pieces, another molecule calledDNA polymerase makes a new strand that matches each of the strands of the split DNA molecule. Each copy of a DNA molecule is made of half of the original (starting) molecule and half of new bases.
When DNA is copied, mistakes are sometimes made – these are calledmutations. There are four main types of mutations:
Deletion, where one or more bases are left out.
Substitution, where one or more bases are substituted for another base in the sequence.
Insertion, where one or more extra base is put in.
Duplication, where a sequence of bases pairs are repeated.
Mutations may also be classified by their effect on the structure and function of proteins, or their effect onfitness. Mutations may be bad for the organism, or neutral, or of benefit. Sometimes mutations are fatal for the organism – the protein made by the new DNA does not work at all, and this causes theembryo to die. On the other hand,evolution is moved forward by mutations, when the new version of the protein works better for the organism.
A section of DNA that contains instructions to make a protein is called agene. Each gene has the sequence for at least onepolypeptide.[6] Proteins form structures, and also form enzymes. The enzymes do most of the work in cells. Proteins are made out of smallerpolypeptides, which are formed ofamino acids. To make a protein to do a particular job, the correct amino acids need to be joined up in the correct order.
Proteins are made by tiny machines in the cell calledribosomes. Ribosomes are in the main body of the cell, but DNA is only in the nucleus of the cell. The codon is part of the DNA, but DNA never leaves the nucleus. Because DNA cannot leave the nucleus, the cell nucleus makes a copy of the DNA sequence inRNA. This is smaller and can get through the holes –pores – in the membrane of the nucleus and out into the cell.
Genes encoded in DNA aretranscribed intomessenger RNA (mRNA) by proteins such asRNA polymerase. Mature mRNA is then used as atemplate for protein synthesis by the ribosome. Ribosomes readcodons, 'words' made of three base pairs that tell the ribosome whichamino acid to add. The ribosome scans along an mRNA, reading the code while it makes protein. Another RNA calledtRNA helps match the right amino acid to each codon.[7]
DNA was first isolated (extracted from cells) bySwissphysician Friedrich Miescher in 1869, when he was working on bacteria from thepus in surgical bandages. The molecule was found in the nucleus of the cells and so he called itnuclein.[8]
In 1928,Frederick Griffith discovered thattraits of the "smooth" form ofPneumococcus could be transferred to the "rough" form of the same bacteria by mixing killed "smooth" bacteria with the live "rough" form.[9] This system provided the first clear suggestion that DNA carries genetic information.
In the 1950s, Erwin Chargaff[13] found that the amount of thymine (T) present in a molecule of DNA was about equal to the amount of adenine (A) present. He found that the same applies to guanine (G) and cytosine (C). Chargaff's rules summarises this finding.
Experimental evidence supporting theWatson andCrick model was published in a series of five articles in the same issue ofNature.[16] Of these, Franklin and Gosling's paper was the first publication of their own X-ray diffraction data and original analysis method that partly supported the Watson and Crick model;[17] this issue also contained an article on DNA structure byMaurice Wilkins and two of his colleagues, whose analysis andin vivo B-DNA X-ray patterns also supported the presencein vivo of the double-helical DNA configurations as proposed by Crick and Watson for their double-helix molecular model of DNA in the previous two pages ofNature. In 1962, after Franklin's death, Watson, Crick, and Wilkins jointly received theNobel Prize inPhysiology or Medicine.[18] Nobel Prizes are awarded only to living recipients. A debate continues about who should receive credit for the discovery.[19]
How DNA was copied (the replication mechanism) came in 1958 through theMeselson–Stahl experiment.[21] More work by Crick and coworkers showed that the genetic code was based on non-overlapping triplets of bases, calledcodons.[22] These findings represent the birth ofmolecular biology.
How Watson and Crick got Franklin's results has been much debated. Crick, Watson andMaurice Wilkins were awarded theNobel Prize in 1962 for their work on DNA – Rosalind Franklin had died in 1958.
DNA gets damaged a lot of times in cells which is a problem has DNA provide instructions to making proteins. But, cells have ways to fix these problems most of the time. Cells make use of special enzymes.[5] Differentenzymes fix different types of damages to DNA. The problem comes in different types:
One commonerror is base mismatch or where the bases are not matched correctly. This is where maybe for example,adenine is not matched withthymine orGuanine is not matched withcytosine. When a cell copies its own DNA a special enzyme calledpolymerase matches the bases together. But once in a while, there is an error. Usually, the enzyme notices it and fixes it, but just make sure, another set of proteins check what the enzyme has done. If the proteins find a base that was not matched with the right base, they remove it and replace it with a nucleotide with the right base.[23]
DNA can also be broken chemically by certaincompounds. This can betoxic compounds like those found intobacco or compounds the cell meets every day likehydrogen peroxide. Some chemical damages by compounds happens so much that there is a special enzyme to fix those types of problems.[23][24]
When aNitrogenous base gets damaged, it is usually fixed in a process calledbase excision repair. Here, an enzyme removes the base and another group of enzymes trim around the damage and replaces it with a new nucleotide.[5]
UV light damages DNA in such a way that it changes its shape. Fixing this type of damage takes a more complex process callednucleotide excision repair. Here, a team of proteins remove a long strand of 20 or more broken nucleotides and replaces them with fresh new ones.[24]
High energy waves likex-rays andgamma rays can actually cut one or both strands of DNA. This type of damage is called a double strand break. One double strand break can cause the cell to die. Two common ways the cell fixes this problem ishomologous recombination andnon homologous end joining. In homologous recombination, enzymes use a similar part of another gene as atemplate to fix the break. In non-homologous end joining enzymes trim around the place where the DNA strand broke and put them together. This way is much less accurate but works when there is no similar genes available.[23]
↑Elgar G. & Vavouri T. 2008. Tuning in to the signals: non-coding sequence conservation in vertebrate genomes.Trends Genet.24 (7): 344–52.doi:10.1016/j.tig.2008.04.005
↑Many complex proteins consist of more than one polypeptide, and the polypeptides are coded separately. They are brought together at a later stage: seeRNA splicing.
↑Fruton, Joseph S. 1999.Proteins, enzymes, genes: the interplay of chemistry and biology. New Haven, Conn: Yale University Press. 438–440ISBN0-300-07608-8
