A 

vitamin is an organic compound required as a nutrient in tiny amounts by an organism.[1] In other

words, an organic chemical compound (or related set of compounds) is called a vitamin when it
cannot be synthesized in sufficient quantities by an organism, and must be obtained from the diet.
Thus, the term is conditional both on the circumstances and on the particular organism. For
example, ascorbic acid (vitamin C) is a vitamin for humans, but not for most other animals, The chemical structure of retinol, the
and biotinand vitamin D are required in the human diet only in certain circumstances. By convention, most common dietary form of
the term vitamin does not include other essential nutrients such as dietary minerals, essential fatty vitamin A
acids, or essential amino acids (which are needed in larger amounts than vitamins), nor does it
encompass the large number of other nutrients that promote health but are otherwise required less often.[2] Thirteen vitamins are presently
universally recognized.
Vitamins are classified by their biological and chemical activity, not their structure. Thus, each "vitamin" refers to a number
ofvitamer compounds that all show the biological activity associated with a particular vitamin. Such a set of chemicals is grouped under an
alphabetized vitamin "generic descriptor" title, such as "vitamin A", which includes the compounds retinal,retinol, and four known carotenoids.
Vitamers by definition are convertible to the active form of the vitamin in the body, and are sometimes inter-convertible to one another, as
well.
Vitamins have diverse biochemical functions. Some have hormone-like functions as regulators of mineral metabolism (e.g., vitamin D), or
regulators of cell and tissue growth and differentiation (e.g., some forms of vitamin A). Others function as antioxidants (e.g., vitamin E and
sometimes vitamin C).[3] The largest number of vitamins (e.g., B complex vitamins) function as precursors for enzyme cofactors, that help
enzymes in their work as catalysts in metabolism. In this role, vitamins may be tightly bound to enzymes as part of prosthetic groups: For
example, biotin is part of enzymes involved in making fatty acids. Vitamins may also be less tightly bound to enzyme catalysts as coenzymes,
detachable molecules that function to carry chemical groups or electrons between molecules. For example, folic acid carries various forms of
carbon group – methyl, formyl, and methylene – in the cell. Although these roles in assisting enzyme-substrate reactions are vitamins' best-
known function, the other vitamin functions are equally important.[4]
Until the mid-1930s, when the first commercial yeast-extract and semi-synthetic vitamin C supplement tablets were sold, vitamins were
obtained solely through food intake, and changes in diet (which, for example, could occur during a particular growing season) can alter the
types and amounts of vitamins ingested. Vitamins have been produced as commodity chemicalsand made widely available as inexpensive
semisynthetic and synthetic-source multivitamin dietary supplements, since the middle of the 20th century.
The term vitamin was derived from "vitamine," a combination word made up by Polish scientist Casimir
Funk from vital and amine, meaning amine of life, because it was suggested in 1912 that the organic micronutrient food factors that prevent
beriberi and perhaps other similar dietary-deficiency diseases might be chemical amines. This proved incorrect for the micronutrient class, and
the word was shortened to vitamin.
History
The discovery dates of the vitamins and their sources
Year of discovery Vitamin Food source
1913 Vitamin A (Retinol) Cod liver oil
1910 Vitamin B1 (Thiamine) Rice bran
1920 Vitamin C (Ascorbic acid) Citrus, most fresh foods
1920 Vitamin D (Calciferol) Cod liver oil
1920 Vitamin B2 (Riboflavin) Meat, eggs
Wheat germ oil, unrefined vegetable
1922 Vitamin E (Tocopherol)
oils
1926  (Cobalamins)
Vitamin B12 liver, eggs, animal products
1929 Vitamin K1 (Phylloquinone) Leafy green vegetables
Meat, whole grains,
1931 Vitamin B5 (Pantothenic acid)
in many foods
1931 Vitamin B7 (Biotin) Meat, dairy products, eggs
1934 Vitamin B6 (Pyridoxine) Meat, dairy products
1936 Vitamin B3 (Niacin) Meat, eggs, grains
1941 Vitamin B9 (Folic acid) Leafy green vegetables
The value of eating a certain food to maintain health was recognized long before vitamins were identified. The ancient Egyptians knew that
feeding liver to a patient would help cure night blindness, an illness now known to be caused by a vitamin A deficiency.[5] The advancement of
ocean voyage during the Renaissance resulted in prolonged periods without access to fresh fruits and vegetables, and made illnesses from
vitamin deficiency common among ships' crews.[6]
In 1749, the Scottish surgeon James Lind discovered that citrus foods helped prevent scurvy, a particularly deadly disease in which collagen is
not properly formed, causing poor wound healing, bleeding of the gums, severe pain, and death.[5] In 1753, Lind published his Treatise on the
Scurvy, which recommended using lemons and limes to avoid scurvy, which was adopted by the British Royal Navy. This led to the
nickname Limey for sailors of that organization. Lind's discovery, however, was not widely accepted by individuals in the Royal
Navy's Arcticexpeditions in the 19th century, where it was widely believed that scurvy could be prevented by practicing good hygiene, regular
exercise, and maintaining the morale of the crew while on board, rather than by a diet of fresh food.[5] As a result, Arctic expeditions continued
to be plagued by scurvy and other deficiency diseases. In the early 20th century, when Robert Falcon Scott made his two expeditions to
the Antarctic, the prevailing medical theory was that scurvy was caused by "tainted" canned food.[5]
During the late 18th and early 19th centuries, the use of deprivation studies allowed scientists to isolate and identify a number of vitamins.
Lipid from fish oil was used to cure rickets in rats, and the fat-soluble nutrient was called "antirachitic A". Thus, the first "vitamin" bioactivity
ever isolated, which cured rickets, was initially called "vitamin A"; however, the bioactivity of this compound is now called vitamin D.[7] In
1881, Russian surgeon Nikolai Lunin studied the effects of scurvy while at the University of Tartu in present-day Estonia.[8] He fed mice an
artificial mixture of all the separate constituents of milk known at that time, namely the proteins,fats, carbohydrates, and salts. The mice that
received only the individual constituents died, while the mice fed by milk itself developed normally. He made a conclusion that "a natural food
such as milk must therefore contain, besides these known principal ingredients, small quantities of unknown substances essential to
life."[8] However, his conclusions were rejected by other researchers when they were unable to reproduce his results. One difference was that
he had used table sugar (sucrose), while other researchers had used milk sugar (lactose) that still contained small amounts of vitamin B.[citation
needed]

The Ancient Egyptians knew that feeding a patient liver (back, right) would help cure night blindness.
In east Asia, where polished white rice was the common staple food of the middle class, beriberi resulting from lack of vitamin B1 was endemic.
In 1884, Takaki Kanehiro, a British trained medical doctor of the Imperial Japanese Navy, observed that beriberi was endemic among low-
ranking crew who often ate nothing but rice, but not among officers who consumed a Western-style diet. With the support of the Japanese
navy, he experimented using crews of twobattleships; one crew was fed only white rice, while the other was fed a diet of meat, fish, barley,
rice, and beans. The group that ate only white rice documented 161 crew members with beriberi and 25 deaths, while the latter group had only
14 cases of beriberi and no deaths. This convinced Takaki and the Japanese Navy that diet was the cause of beriberi, but mistakenly believed
that sufficient amounts of protein prevented it.[9] That diseases could result from some dietary deficiencies was further investigated
by Christiaan Eijkman, who in 1897 discovered that feeding unpolished riceinstead of the polished variety to chickens helped to prevent
beriberi in the chickens. The following year, Frederick Hopkins postulated that some foods contained "accessory factors" — in addition to
proteins, carbohydrates, fats, et cetera — that are necessary for the functions of the human body.[5] Hopkins and Eijkman were awarded
the Nobel Prize for Physiology or Medicine in 1929 for their discovery of several vitamins.[10]
In 1910, the first vitamin complex was isolated by Japanese scientist Umetaro Suzuki, who succeeded in extracting a water-soluble complex of
micronutrients from rice bran and named it aberic acid (later Orizanin). He published this discovery in a Japanese scientific journal.[11] When the
article was translated into German, the translation failed to state that it was a newly discovered nutrient, a claim made in the original Japanese
article, and hence his discovery failed to gain publicity. In 1912 Polish biochemist Casimir Funk isolated the same complex of micronutrients and
proposed the complex be named "vitamine" (a portmanteau of "vital amine").[12] The name soon became synonymous with Hopkins' "accessory
factors", and, by the time it was shown that not all vitamins are amines, the word was already ubiquitous. In 1920, Jack Cecil
Drummond proposed that the final "e" be dropped to deemphasize the "amine" reference, after researchers began to suspect that not all
"vitamines" (in particular, vitamin A) has an amine component.[9]
In 1931, Albert Szent-Györgyi and a fellow researcher Joseph Svirbely suspected that "hexuronic acid" was actually vitamin C, and gave a sample
to Charles Glen King, who proved its anti-scorbutic activity in his long-established guinea pig scorbutic assay. In 1937, Szent-Györgyi was
awarded the Nobel Prize in Physiology or Medicine for his discovery. In 1943,Edward Adelbert Doisy and Henrik Dam were awarded the Nobel
Prize in Physiology or Medicine for their discovery of vitamin K and its chemical structure. In 1967, George Wald was awarded the Nobel Prize
(along with Ragnar Granit and Haldan Keffer Hartline) for his discovery that vitamin A could participate directly in a physiological process.[10]
In humans
Vitamins are classified as either water-soluble or fat-soluble. In humans there are 13 vitamins: 4 fat-soluble (A, D, E, and K) and 9 water-soluble
(8 B vitamins and vitamin C). Water-soluble vitamins dissolve easily in water and, in general, are readily excreted from the body, to the degree
that urinary output is a strong predictor of vitamin consumption.[13] Because they are not readily stored, consistent daily intake is important.
[14]
 Many types of water-soluble vitamins are synthesized by bacteria.[15] Fat-soluble vitamins are absorbed through theintestinal tract with the
help of lipids (fats). Because they are more likely to accumulate in the body, they are more likely to lead to hypervitaminosis than are water-
soluble vitamins. Fat-soluble vitamin regulation is of particular significance in cystic fibrosis.[16]
List of vitamins
Each vitamin is typically used in multiple reactions, and, therefore, most have multiple functions.[17]
Vitamin Recommende Upper
generic
Vitamer chemical name(s) (list not complete) Solubilit d dietary Intake
descripto allowances Deficiency disease Level Overdose disease
r name y (male, age (UL/day)
19–70)[18] [18]

Retinol, retinal, and Night-blindness, Hyper

Vitamin Hypervitaminosis
four carotenoids Fat 900 µg keratosis, 3,000 µg
A A
including beta carotene and Keratomalacia[19]
Drowsiness or
Beriberi, Wernicke- [20] muscle relaxation
Vitamin B1 Thiamine Water 1.2 mg N/D
Korsakoff syndrome with large doses.
[21]

Vitamin B2 Riboflavin Water 1.3 mg Ariboflavinosis N/D

Vitamin B3 Niacin, niacinamide Water 16.0 mg Pellagra 35.0 mg Liver damage
(doses > 2g/day)
[22]
 andother
problems
Diarrhea; possibly
Vitamin B5 Pantothenic acid Water 5.0 mg[23] Paresthesia N/D nausea and
heartburn.[24]
Impairment
[25] of proprioception
Anemia  peripheral
Vitamin B6 Pyridoxine,pyridoxamine,pyridoxal Water 1.3–1.7 mg 100 mg , nerve damage
neuropathy.
(doses >
100 mg/day)
Vitamin B7 Biotin Water 30.0 µg Dermatitis, enteritis N/D
Megaloblast and May mask
Deficiency during symptoms of
Vitamin B9 Folic acid, folinic acid Water 400 µg pregnancy is associated 1,000 µg vitamin
with birth defects, such B12deficiency; oth
as neural tube defects er effects.
Acne-like rash
Cyanocobalamin,hydroxycobalamin,methylcobal Megaloblastic [causality is not
Vitamin B12 Water 2.4 µg N/D
amin anemia[26] conclusively
established].
Vitamin Vitamin C
Ascorbic acid Water 90.0 mg Scurvy 2,000 mg
C megadosage
Vitamin 5.0 µg–10 µ Rickets and Osteomala Hypervitaminosis
Ergocalciferol,cholecalciferol Fat 50 µg
D g[27] cia D
Increased
Deficiency is very rare; congestive heart
mildhemolytic failure seen in
Vitamin E Tocopherols,tocotrienols Fat 15.0 mg 1,000 mg
anemia in newborn one large
infants.[28] randomized
study.[29]
Increases
Vitamin coagulation in
phylloquinone,menaquinones Fat 120 µg Bleeding diathesis N/D
K patients
takingwarfarin.[30]
In nutrition and diseases
Vitamins are essential for the normal growth and development of a multicellular organism. Using the genetic blueprint inherited from its
parents, a fetus begins to develop, at the moment of conception, from the nutrients it absorbs. It requires certain vitamins and minerals to be
present at certain times. These nutrients facilitate the chemical reactions that produce among other things, skin, bone, and muscle. If there is
serious deficiency in one or more of these nutrients, a child may develop a deficiency disease. Even minor deficiencies may cause permanent
damage.[31]
For the most part, vitamins are obtained with food, but a few are obtained by other means. For example, microorganisms in the intestine —
commonly known as "gut flora" — produce vitamin K and biotin, while one form of vitamin D is synthesized in the skin with the help of the
natural ultraviolet wavelength of sunlight. Humans can produce some vitamins from precursors they consume. Examples include vitamin A,
produced from beta carotene, and niacin, from the amino acid tryptophan.[18]
Once growth and development are completed, vitamins remain essential nutrients for the healthy maintenance of the cells, tissues, and organs
that make up a multicellular organism; they also enable a multicellular life form to efficiently use chemical energy provided by food it eats, and
to help process the proteins, carbohydrates, and fats required for respiration.[3]
Deficiencies
It was suggested that, when plants and animals began to transfer from the sea to rivers and land about 500 million years ago, environmental
deficiency of marine mineral antioxidants was a challenge to the evolution of terrestrial life. Terrestrial plants slowly optimized the production
of “new” endogenous antioxidants such as ascorbic acid (Vitamin C), polyphenols, flavonoids, tocopherols, etc. Since this age, dietary vitamin
deficiencies appeared in terrestrial animals.[32] Humans must consume vitamins periodically but with differing schedules, to avoid deficiency.
Human bodily stores for different vitamins vary widely; vitamins A, D, and B12 are stored in significant amounts in the human body, mainly in
the liver,[28] and an adult human's diet may be deficient in vitamins A and D for many months and B12 in some cases for years, before developing
a deficiency condition. However, vitamin B3 (niacin and niacinamide) is not stored in the human body in significant amounts, so stores may last
only a couple of weeks.[19][28] For vitamin C, the first symptoms of scurvy in experimental studies of complete vitamin C deprivation in humans
have varied widely, from a month to more than six months, depending on previous dietary history that determined body stores.[33]
Deficiencies of vitamins are classified as either primary or secondary. A primary deficiency occurs when an organism does not get enough of
the vitamin in its food. A secondary deficiency may be due to an underlying disorder that prevents or limits the absorption or use of the
vitamin, due to a “lifestyle factor”, such as smoking, excessive alcohol consumption, or the use of medications that interfere with the
absorption or use of the vitamin.[28] People who eat a varied diet are unlikely to develop a severe primary vitamin deficiency. In contrast,
restrictive diets have the potential to cause prolonged vitamin deficits, which may result in often painful and potentially deadly diseases.
Well-known human vitamin deficiencies involve thiamine (beriberi), niacin (pellagra), vitamin C (scurvy), and vitamin D (rickets). In much of the
developed world, such deficiencies are rare; this is due to (1) an adequate supply of food and (2) the addition of vitamins and minerals to
common foods, often called fortification.[18][28] In addition to these classical vitamin deficiency diseases, some evidence has also suggested links
between vitamin deficiency and a number of different disorders.[34][35]
Side-effects and overdose
In large doses, some vitamins have documented side-effects that tend to be more severe with a larger dosage. The likelihood of consuming too
much of any vitamin from food is remote, but overdosing (vitamin poisoning) from vitamin supplementation does occur. At high enough
dosages, some vitamins cause side-effects such as nausea, diarrhea, and vomiting.[19][36]When side-effects emerge, recovery is often
accomplished by reducing the dosage. The doses of vitamins different individual can tolerate varies widely, and appear to be related to age and
state of health.[37]
In 2008, overdose exposure to all formulations of vitamins and multivitamin-mineral formulations was reported by 68,911 individuals to
the American Association of Poison Control Centers(nearly 80% of these exposures were in children under the age of 6), leading to 8 "major"
life-threatening outcomes and 0 deaths.[38]
Supplements
Dietary supplements, often containing vitamins, are used to ensure that adequate amounts of nutrients are obtained on a daily basis, if optimal
amounts of the nutrients cannot be obtained through a varied diet. Scientific evidence supporting the benefits of some vitamin supplements is
well established for certain health conditions, but others need further study.[39]In some cases, vitamin supplements may have unwanted effects,
especially if taken before surgery, with other dietary supplements or medicines, or if the person taking them has certain health conditions.
[39]
 Dietary supplements may also contain levels of vitamins many times higher, and in different forms, than one may ingest through food.[40]
There have been mixed studies on the importance and safety of dietary supplementation. A meta-analysis published in 2006 suggested that
Vitamin A and E supplements not only provide no tangible health benefits for generally healthy individuals but may actually increase mortality,
although two large studies included in the analysis involved smokers, for which it was already known that beta-carotene supplements can be
harmful.[41] Another study published in May 2009 found that antioxidants such as vitamins C and E may actually curb some benefits of exercise.
[42]
 While others findings suggest that evidence of Vitamin E toxicity is limited to specific form taken in excess.[43]
Governmental regulation of vitamin supplements
Most countries place dietary supplements in a special category under the general umbrella of foods, not drugs. This necessitates that the
manufacturer, and not the government, be responsible for ensuring that its dietary supplement products are safe before they are marketed.
Regulation of supplements varies widely by country. In the United States, a dietary supplement is defined under the Dietary Supplement Health
and Education Act of 1994.[44] In addition, the Food and Drug Administration uses the Adverse Event Reporting System to monitor adverse
events that occur with supplements.[45] In the European Union, the Food Supplements Directive requires that only those supplements that have
been proven safe can be sold without a prescription.[46]
Names in current and previous nomenclatures
Nomenclature of reclassified vitamins
Previous name Chemical name Reason for name change[47]
Vitamin B4 Adenine DNA metabolite; synthesized in body
Vitamin B8 Adenylic acid DNA metabolite; synthesized in body
Needed in large quantities (does
Vitamin F Essential fatty acids
not fit the definition of a vitamin).
Vitamin G Riboflavin Reclassified as Vitamin B2
Vitamin H Biotin Reclassified as Vitamin B7
Vitamin J Catechol, Flavin Catechol nonessential; flavin reclassified as B2
[48]
Vitamin L 1 Anthranilic acid Non essential
Adenylthiomethylpentos
Vitamin L2[48] RNA metabolite; synthesized in body
e
Vitamin M Folic acid Reclassified as Vitamin B9
Vitamin O Carnitine Synthesized in body
Vitamin P Flavonoids No longer classified as a vitamin
Vitamin PP Niacin Reclassified as Vitamin B3
Proposed inclusion[49] of salicylate as an essential
Vitamin S Salicylic acid
micronutrient
Vitamin U S-Methylmethionine Protein metabolite; synthesized in body
The reason that the set of vitamins skips directly from E to K is that the vitamins corresponding to letters F-J were either reclassified over time,
discarded as false leads, or renamed because of their relationship to vitamin B, which became a complex of vitamins.
The German-speaking scientists who isolated and described vitamin K (in addition to naming it as such) did so because the vitamin is intimately
involved in the Koagulation of blood following wounding. At the time, most (but not all) of the letters from F through to J were already
designated, so the use of the letter K was considered quite reasonable.[47][50] The table on the right lists chemicals that had previously been
classified as vitamins, as well as the earlier names of vitamins that later became part of the B-complex.
Anti-vitamins
Main article: Antinutrient
Anti-vitamins are chemical compounds that inhibit the absorption or actions of vitamins. For example, avidin is a protein in egg whites that
inhibits the absorption of biotin.[51] Pyrithiamine is similar to thiamine vitamin B1 and inhibits the enzymes that use thiamine.[52]

DNA Replication in Prokaryotes

 
Introduction

DNA replication has turned  

out to be a much more
complex process
Steps than we
in DNA
originally thought. Some
Replication inof
this complexity arises
Prokaryotes: E. coli
because of two reasons
which you should keep in
mind: Initiation

1. The DNA 1. molecule

Original DNA is molecule.
antiparallel, meaning that the and are
The parent strands
shownofinthe
strand or halves red.
molecule are orientedproteins
2. Initiator in attach to a
opposite directions. In this site,
specific initiation
diagram therecognized
left strandas a particular
(reading here from top
sequence to nucleotides.
of DNA
bottom) is the 5'---> 3' strand
and the right strand
3. DNA is the attaches at
Helicase
3'---> 5' strand.
initiation site. Other proteins
called SSB(single strand binding
2. The enzymes which
proteins), lay reannealing
prevent
down the complementary
of the DNA.
strand to each parent strand
only travels in a 3' ---> 5'
DNA Helicase is an enzyme
direction relative to the
that unravels the DNA
parent strand. 
double helix and breaks the
hydrogen bonds.
So DNA synthesis in the left
hand strand4.of Replication fork formation.
my diagram
would be from bottom to top
of the page,Replication
whereas DNA fork. The
synthesis using the right refers to the
replication fork
hand strandregion
wouldonbethe DNA that is
from
top to bottom since for the of DNA
the leading edge
right hand replication
strand this as the DNA
corresponds to thein3'a--->5'
unzips particular region.
direction. At this stage the replication
fork has a complex of
Note that theproteins including the
new strand
enzyme
itself is growing helicase
from its 5' and another
enzyme,
end to its 3' end.  DNA primase.

DNA primase is an enzyme

    that generates an RNA
sequence that serves as a
starting point or primer for
synthesis of the new DNA
chain. 
5. Start of DNA synthesis on
leading strand of DNA using
DNA polymerases. 

DNA polymerases are
enzymes that synthesize a
complementary DNA strand
using a the original strand as
a template.  In DNA
synthesis the new strand
grows 5' to 3'.
Elongation

1. Production of new DNA

half from parental leading
strand as a template.
Remember that DNA
synthesis is in 3' --> 5'
direction of the parental
strand. Leading strand
synthesis is continuous from
the primer to the replication
fork. 

Meanwhile another RNA

primase(Light brown) has
attached an RNA
primer(Purple) to the upper
parental strand. This other
new strand is the lagging
strand. It's synthesis is
discontinuous.
2. Production of first Okazaki
fragment in the lagging strand

An Okazaki fragment(a) is a
stretch of non parental DNA
produced along the lagging
strand of parental DNA by
the DNA polymerase
beginning at primer(b). Since
the initiator proteins do not
move at this stage, the DNA
polymerase has to stop
synthesis when it is
encountered. Primer(c) is
shown being synthesized by
the DNA primase.
3. Production of of more
Okazaki fragments and joining
of fragments using ligase.

Synthesis of DNA along the

leading strand still continues
and multiple Okazaki
fragments are produced by
DNA polymerase III. Once
several fragments are
produced, the primer is
removed by another DNA
polymerase called DNA
polymerase I 1 (b). Then
another enzyme, a ligase
joins the DNA fragments
together (a). 

This process continues until

all the DNA is replicated.
Bi-directional
synthesis
In many prokaryotes two
replication forks develop
from at the initiation site,
each initiation fork traveling
in opposite directions as
shown here. Thus, what
strand is lagging or leading
depends on which replication
fork you are dealing with!    

  
 

Steps of DNA Replication

The next we have to do is to shed light into the mystery of the steps of DNA Replicationof the Eykaryotes. 

1)The first major step for the DNA Replication to take place is the breaking of hydrogen bonds between bases of the two antiparallel strands. The unwounding of the two
strands is the starting point. The splitting happens in places of the chains which are rich in A-T. That is because there are only two bonds between Adenine and Thymine (there
are three hydrogen bonds between Cytosine and Guanine). Helicase is the enzyme that splits the two strands. The initiation point where the splitting starts is called "origin of
replication".The structure that is created is known as "Replication Fork".
2) One of the most important steps of DNA Replication is the binding of RNA Primase in the the initiation point of the 3'-5' parent chain. RNA Primase can attract RNA
nucleotides which bind to the DNA nucleotides of the 3'-5' strand due to the hydrogen bonds between the bases. RNA nucleotides are the primers (starters) for the binding of
DNA nucleotides. 

3) The elongation process is different for the 5'-3' and 3'-5' template. a)5'-3' Template: The 3'-5' proceeding daughter strand -that uses a 5'-3' template- is called leading
strand because DNA Polymerase ä can "read" the template and continuously adds nucleotides (complementary to the nucleotides of the template, for example Adenine
opposite to Thymine etc). 
b)3'-5'Template: The 3'-5' template cannot be "read" by DNA Polymerase ä. The replication of this template is complicated and the new strand is called lagging strand. In the
lagging strand the RNA Primase adds more RNA Primers. DNA polymerase å reads the template and lengthens the bursts. The gap between two RNA primers is called
"Okazaki Fragments". 

The RNA Primers are necessary for DNA Polymerase å to bind Nucleotides to the 3' end of them. The daughter strand is elongated with the binding of more DNA nucleotides. 

4) In the lagging strand the DNA Pol I -exonuclease- reads the fragments and removes the RNA Primers. The gaps are closed with the action of DNA Polymerase (adds
complementary nucleotides to the gaps) and DNA Ligase (adds phosphate in the remaining gaps of the phosphate - sugar backbone). 

Each new double helix is consisted of one old and one new chain. This is what we call semiconservative replication.
5) The last step of DNA Replication is the Termination. This process happens when the DNA Polymerase reaches to an end of the strands. We can easily understand that in
the last section of the lagging strand, when the RNA primer is removed, it is not possible for the DNA Polymerase to seal the gap (because there is no primer). So, the end of
the parental strand where the last primer binds isn't replicated. These ends of linear (chromosomal) DNA consists of noncoding DNA that contains repeat sequences and are
called telomeres. As a result, a part of the telomere is removed in every cycle of DNA Replication. 

6) The DNA Replication is not completed before a mechanism of repair fixes possible errors caused during the replication. Enzymes like nucleases remove the wrong
nucleotides and the DNA Polymerase fills the gaps.

Similar processes also happen during the steps of DNA Replication of prokaryotes though there are some differences.