Information

Why does DNA have its name?

Why does DNA have its name?


We are searching data for your request:

Forums and discussions:
Manuals and reference books:
Data from registers:
Wait the end of the search in all databases.
Upon completion, a link will appear to access the found materials.

Why is DNA called deoxyribonucleic acid and not something else? I get the nucleic acid part (because that's what DNA is made of) but what about the deoxyribo- part, especially the ribo- part. Maybe because DNA doesn't have oxygen, hence the "deoxy-"?

(Also, please tell me what is wrong with my question or whether there was a duplicate I didn't find so I can fix this question or delete it.)


The name is derived from the sugar which is bound to the base. For RNA it is Ribose (that why it is called ribonucleic acid) and for DNA it is Deoxyribose (hence the name deoxynucleic acid). The deoxyribose is missing an OH-group at positition 2 of the sugar ring, the name literally means "without oxygen". See the image below (from here) for further clarification:


Why Is DNA Double Stranded? The Discovery of DNA Excision Repair Mechanisms

The persistence of hereditary traits over many generations testifies to the stability of the genetic material. Although the Watson–Crick structure for DNA provided a simple and elegant mechanism for replication, some elementary calculations implied that mistakes due to tautomeric shifts would introduce too many errors to permit this stability. It seemed evident that some additional mechanism(s) to correct such errors must be required. This essay traces the early development of our understanding of such mechanisms. Their key feature is the cutting out of a section of the strand of DNA in which the errors or damage resided, and its replacement by a localized synthesis using the undamaged strand as a template. To the surprise of some of the founders of molecular biology, this understanding derives in large part from studies in radiation biology, a field then considered by many to be irrelevant to studies of gene structure and function. Furthermore, genetic studies suggesting mechanisms of mismatch correction were ignored for almost a decade by biochemists unacquainted or uneasy with the power of such analysis. The collective body of results shows that the double-stranded structure of DNA is critical not only for replication but also as a scaffold for the correction of errors and the removal of damage to DNA. As additional discoveries were made, it became clear that the mechanisms for the repair of damage were involved not only in maintaining the stability of the genetic material but also in a variety of biological phenomena for increasing diversity, from genetic recombination to the immune response.

THE Austrian theoretical physicist, Erwin Schrödinger, one of the inventors of wave mechanics, was fascinated by the Hapsburg lip, a distinctive facial feature of the Hapsburg imperial family. This was not only because he was Austrian but, as a physicist trying to understand biology, he was fascinated by the stability of this trait over the centuries, something that seemed to defy the laws of thermodynamics (Schrödinger 1945). Geneticists and biochemists in the 1940s were comparably impressed by the apparent removal of DNA from the hurly-burly of cellular metabolism, a property that one might associate with such hereditary stability (Mazia 1952).

A major step forward in understanding the properties of the genetic material was the formulation of the double-stranded structure of DNA by James Watson and Francis Crick in 1953, which suggested a mechanism for its replication and accordingly its perpetuation. In one of the more famous understatements in the scientific literature they wrote: “It has not escaped our attention that the specific pairing we have postulated immediately suggests a possible copying mechanism for the genetic material” (Watson and Crick 1953a,b). What apparently did escape their attention, and that of the early molecular biologists, was that this double-stranded structure also served as a safety device, permitting the repair of damage to one or the other of the strands. Even more surprising, in hindsight at least, was that this recognition first came from what was then the unfashionable field of radiation biology.

Today the subject of DNA repair is a fully accepted part of the body of contemporary molecular knowledge. Current textbooks of molecular biology, genetics, and biochemistry list DNA repair mechanisms comfortably among the multitude of metabolic pathways. Table 1 summarizes the ones discussed in this article. Manipulation of these pathways is central to the application of CRISPR, perhaps the most productive of recent biological technologies and the latest major addition to the field of DNA repair. The Nobel Prize in chemistry for 2015 was awarded to Tomas Lindahl, Paul Modrich, and Aziz Sancar for their detailed mechanistic studies on repair, which is confirmation of the current respectability of studies on DNA repair.

Yet it is clear that the early workers in this field were justified in feeling that their work was not given the recognition it deserved as a key factor in the DNA-centered view of life that became the science of molecular biology. John Cairns, a key figure in that development, writing as late as in 2008, was able to trace the foundations of molecular biology and list its exciting discoveries without mentioning the fact that DNA could be repaired (Cairns 2008). A review on the history of “target theory” (a pioneering, somewhat earlier, attempt to understand the biological effects of radiation) (Box 1) reports: “Around 30 years ago, a very prominent molecular biologist confidently proclaimed that nothing of fundamental importance has ever been learned by irradiating cells!” (Bedford and Dewey 2002 J. S. Bedford, personal communication). What was the basis for this attitude and what produced the change?

The introduction of ionizing radiation as a tool in the 1920s and 1930s led to major advances in our understanding of the gene. The discovery by Muller (1927) and almost simultaneously by Stadler (1928a,b) that ionizing radiation could produce mutations in what had hitherto been an impenetrable gene opened up the possibility of actually investigating the properties of this biological entity by physical means. Further investigations by Timofeeff-Ressovsky et al. (1935) led to the hypothesis that the “gene” was a molecule and to a calculation of its possible size that was/is reasonable. This “three-man article” found its way to Schrödinger (1945) who made Delbrück’s model a key feature of his book What is Life?, a work which enticed many of its founders into what became molecular biology.

The advantage and disadvantage of radiation is that it lent itself to quantitative studies and to a mathematical analysis of the results obtained. The result was target theory: the idea that the gene, or virus, was a target at which quantum bullets could be shot. There was then a relationship between the size of the target and the number (dose) of bullets that needed to be shot at random to hit the target. The hypothesis was reasonable as a first approximation and was developed to a high degree of sophistication (Lea 1946). The hypothesis had many failings but, to my mind, a major one was the concentration of research on the absolute linear dependence of the mutation rate on dose. There were political and social reasons for this concentration in a world attempting to come to terms with the development of atomic energy. One scientific result was a concentration of radiation research on the interpretation of killing curves with different types of radiation being applied at differing dose rates and with different end points. At no point was this research able to identify the target molecule. Notwithstanding really sophisticated analysis, this research did not provide as much insight as subsequent biochemical analysis.


DNA breakthrough could identify why some are more affected by COVID-19

Credit: Shutterstock

Scientists from the MRC Weatherall Institute of Molecular Medicine at Oxford University have developed a method that allows them to see, with far greater accuracy, how DNA forms large scale structures within a cell nucleus.

This breakthrough will improve understanding of how differences in DNA sequences can lead to increased risks of developing many different diseases.

The method, which is around 1000 times more accurate than existing techniques, enables scientists to measure the contacts between different pieces of DNA, which are a million base pairs apart to the nearest base pair. This is the equivalent of being able to measure contacts in the DNA fiber that are 1km apart to the nearest millimeter.

Put another way, if each letter of DNA was the size of a brick, each cell would contain roughly the number of bricks in a city (6 billion). Scientists are now able to work out which bricks are next to each other, and see the fine details of how DNA forms structures inside cells, when previously they could only see the DNA "architecture" on the scale of small buildings.

Associate Professor James Davies, the MRC clinician scientist at the Radcliffe Department of Medicine who led the research, explains, "This technique has real potential to make a significant impact on human health. For example, at the moment we know that there is a genetic variant which doubles the risk of being severely affected by COVID-19. However, we do not know how the genetic variant makes people more vulnerable to COVID-19.

"This new breakthrough is helping us to work out how this causes severe COVID and which genes are involved. This is important because we know that drugs which are developed to targets with this type of genetic evidence have double the chance of making it past early stage clinical trials. The team is now using the technique to make the genetic identification and hopes to report on results in coming weeks."


You Can See Why DNA Is Important

Dr. Francis Collins, director of the Human Genome Project (that mapped the human DNA structure) said that one can "think of DNA as an instructional script, a software program, sitting in the nucleus of the cell." 5

Perry Marshall, an information specialist, comments on the implications of this. "There has never existed a computer program that wasn't designed. [whether it is] a code, or a program, or a message given through a language, there is always an intelligent mind behind it." 6

Just as former atheist Dr. Antony Flew questioned, it is legitimate to ask oneself regarding this three billion letter code instructing the cell. who wrote this script? Who placed this working code, inside the cell?

It's like walking along the beach and you see in the sand, "Mike loves Michelle." You know the waves rolling up on the beach didn't form that--a person wrote that. It is a precise message. It is clear communication. In the same way, the DNA structure is a complex, three-billion-lettered script, informing and directing the cell's process.

How can one explain this sophisticated messaging, coding, residing in our cells?

On June 26, 2000, President Clinton congratulated those who completed the human genome sequencing. President Clinton said, "Today we are learning the language in which God created life. We are gaining ever more awe for the complexity, the beauty, the wonder of God's most divine and sacred gift." 7 Dr. Francis Collins, director of the Human Genome Project, followed Clinton to the podium stating, "It is humbling for me and awe inspiring to realize that we have caught the first glimpse of our own instruction book, previously known only to God." 8

When looking at the DNA structure within the human body, we cannot escape the presence of intelligent (incredibly intelligent) design.

According to the Bible (which is itself incredibly complex) God is not only the Author of our existence, but he is the Relationship that makes our existence meaningful. All the intangibles in life that we crave. enough strength for any situation, joy, wisdom, and knowing we are loved. God alone gives these to us as we listen to him and trust him. He is our greatest, reliable guide in life. Just as he has engineered DNA to instruct the cell, he offers to instruct us to make our lives function well, for his glory and for our sake, because he loves us.

Why is DNA important? It's one more proof for God. He designed our bodies. He can also be trusted to design your life. Have you ever begun a relationship with God? This explains how you can: Knowing God Personally.

For further evidence that seeks to answer the question, "Is God real?" please see Is There a God?


Why does DNA have its name? - Biology

Deoxyribonucleic acid (DNA) is a nucleic acid that contains the genetic instructions for the development and function of living things.

All known cellular life and some viruses contain DNA.

The main role of DNA in the cell is the long-term storage of information.

It is often compared to a blueprint, since it contains the instructions to construct other components of the cell, such as proteins and RNA molecules.

The DNA segments that carry genetic information are called genes, but other DNA sequences have structural purposes, or are involved in regulating the expression of genetic information.

In eukaryotes such as animals and plants, DNA is stored inside the cell nucleus, while in prokaryotes such as bacteria and archaea, the DNA is in the cell's cytoplasm.

Unlike enzymes, DNA does not act directly on other molecules rather, various enzymes act on DNA and copy its information into either more DNA, in DNA replication, or transcribe it into protein.

Other proteins such as histones are involved in the packaging of DNA or repairing the damage to DNA that causes mutations.

DNA is a long polymer of simple units called nucleotides, which are held together by a backbone made of sugars and phosphate groups.

This backbone carries four types of molecules called bases and it is the sequence of these four bases that encodes information.

The major function of DNA is to encode the sequence of amino acid residues in proteins, using the genetic code.

To read the genetic code, cells make a copy of a stretch of DNA in the nucleic acid RNA.

These RNA copies can then used to direct protein synthesis, but they can also be used directly as parts of ribosomes or spliceosomes.


DNA REPLICATION

Replication is the process where DNA makes a copy of itself. Why does DNA need to copy? Simple: Cells divide for an organism to grow or reproduce, every new cell needs a copy of the DNA or instructions to know how to be a cell. DNA replicates right before a cell divides.

DNA replication is semi-conservative. That means that when it makes a copy, one half of the old strand is always kept in the new strand. This helps reduce the number of copy errors.


Why Does DNA Need to Replicate?

DNA replicates to make copies of itself. This is an indispensable process that allows cells to divide for a living organism to grow or reproduce. Each new cell needs a DNA copy, which serves as instructions on how to function as a cell.

DNA replicates before a cell divides. The replication process is semi-conservative, which means that when DNA creates a copy, half of the old strand is retained in the new strand to reduce the number of copy errors. DNA contains the code for building an organism and making sure that the organism functions properly. For this reason, DNA is often called the blueprint of life. Its function is comparable to a builder using a blueprint to make a house. The blueprint contains all of the necessary plans and instructions for the organism. It brings the information for making a cell&rsquos proteins, which are responsible for implementing the functions of an organism and determining the organism&rsquos characteristics. After reproducing, the cell passes this crucial information to the daughter cells. DNA replication occurs in the nucleus of eukaryotes and the cytoplasm of prokaryotes. The replicating process is the same, regardless of where it takes place. Various kinds of cells replicate their DNA at different rates. Some undergo several rounds of cell division, such as those in a human&rsquos heart and brain, while other cells constantly divide, like those in the fingernails and hair.


How is DNA passed on to the next generation?^

When humans reproduce, they pass on their genetic information to their offspring. However, if each parent passed on his or her entire genetic code, their child would have twice as many chromosomes as each parent. If this pattern were to continue, the number of chromosomes would double each and every generation, which would quickly become unworkable for cells. In order for a baby to have a non-increasing number of chromosomes, he or she must receive half the normal number of chromosomes from each parent. Therefore, the reproductive cells known as eggs in adult females and sperm in adult males&ndashcollectively termed germ cells&ndashmust have only half the normal number of chromosomes. Hence, gametes have only 23 chromosomes instead of 23 pairs (46 chromosomes total) like the rest of the cells in your body. These cells are called haploid, as opposed to cells with two pairs of each chromosome that are called diploid.

A special kind of cell division called meiosis generates haploid gametes from diploid parental cells. Meiosis occurs only for the formation of eggs and sperm, but it is clearly a very important process. To get daughter cells with half the number of chromosomes, cells replicate their DNA and then divide twice, instead of once as in mitosis. The result is four daughter cells that are normally genetically different from the parent cell and from each other.

Before we start describing the phases of meiosis, let&rsquos take a moment to clarify the concepts regarding homologous chromosomes and sister chromatids. Homologous chromosomes each have the same type of information, but one was inherited from your mother and the other was inherited from your father. In other words, at the same location or &ldquogene locus&rdquo on each homologous chromosome is the gene for a certain trait, such as eye color. Because each homologous chromosome comes from a different parent, however, the alleles, or versions of the gene, can be different. You could get a blue-eyed allele from your father and a brown-eyed allele from your mother, for example. Sister chromatids, on the other hand, only form once a cell has replicated its DNA. They are two identical copies of one chromosome, joined at the middle to form the familiar X-shape. Sister chromatids are pulled apart during mitosis (and, as we will see, during the second phase of meiosis). To summarize: each chromosome has a matching homologue, which carries similar but not identical information. A pair of identical sister chromatids is the result of a chromosome replicating itself.

Now we can begin with a closer look at meiosis. Cells that undergo meiosis first have an interphase, during which they replicate their DNA, followed by two special rounds of cell division. The stages of division have the same names as in mitosis, but are distinguished from each other by roman numerals: the first round, meiosis I, consists of prophase I, metaphase I, etc. and the second round, meiosis II, consists of prophase II, metaphase II, etc. The second division proceeds a lot like mitosis, with the separation of sister chromatids. The first division, however, is different from mitosis in important ways, as we will see.

Prophase I is more complex than mitosis prophase (or prophase II of meiosis). In prophase I, the X-shaped chromosomes (pairs of sister chromatids) also become visible, but this time homologous chromosomes pair up instead of remaining independent. Each pair is held tightly together, forming what is called a bivalent and allowing a process called &ldquocrossing over&rdquo to take place. Crossing over is a very important phenomenon in genetics. When chromosomes overlap, genetic material from one chromosome (inherited from the mother, say) can trade places with genetic material from the other chromosome (inherited from the father). For example, your mother&rsquos brown-eyed allele could switch places with your father&rsquos blue-eyed one. This process shuffles the genetic information, creating chromosomes that are unique combinations of maternal and paternal alleles, and not just copies from one parent or the other. For this reason, crossing over is said to promote genetic recombination. Crossing over is an important source of genetic variation, which helps make every single person genetically unique (unless you have an identical twin). Interestingly, cells can remain in this state of paired homologous chromosomes for a very long time, even for years. For example, a female baby&rsquos reproductive cells begin meiosis before she is born, but they only progress as far as prophase I. Meiosis later resumes when she reaches puberty.

At the start of prometaphase I, the nuclear membrane breaks down and microtubules attach to the chromosomes, just like in mitotic prometaphase, and meiosis I proceeds. In metaphase I, all the bivalents line up on the equator of the cell. Then, during anaphase I, the homologues are pulled apart as the attached microtubules shorten and the centrosomes move outward. The cell then continues to divide until there are two daughter cells, marking the end of meiosis I.

Before the start of meiosis II, DNA replication does not occur. Instead, meiosis II begins like mitosis, with the chromosomes (still in the form of paired sister chromatids) lining up at the equator of the cell. They are then pulled apart by the microtubules, and the cell divides in two. The result of meiosis II is that now we have only 23 chromosomes in each daughter cell, whereas in mitosis there were a full 46 chromosomes in each daughter cell. Remember that at the beginning of meiosis II there are two cells each undergoing a division, so the final product will be four daughter cells. Observe that there are only 23 chromosomes (the haploid number) in each resulting germ cell and how each one has a unique combination of chromosomes.


What Does DNA Tell Us About Race?

Today is National DNA Day, a day to commemorate the publication of James Watson and Francis Crick’s famous paper (that included the work of Rosalind Franklin) in 1953 describing the structure of DNA. As we reflect back on the incredible scientific progress that has been made since this paper, one of the most striking developments is how the study of our own genomes has changed our understanding of human variation

The American Association of Physical Anthropologists, an organization of scientists dedicated to the study of the biological variation, adaptation, and evolution of humans and our close relatives, has just released a position statement on race and racism. It provides a nice insight into what has been learned about patterns of genetic and phenotypic variation in human populations since the publication of Watson and Crick’s paper 66 years ago.

Professor Robin Nelson (Santa Clara University), who was involved in writing the statement, commented, "The AAPA has a responsibility to provide scientifically accurate information to the public about race and racism. This statement reflects our commitment to engaging in these sometimes difficult conversations."

Race is not a biologically meaningful category

As the statement discusses, one of the most important insights from studies of human DNA across the world has been that the concept of “race” is not a useful or accurate term to describe patterns of biological variation that exist. Biological variation—whether it be genetic or in our physical traits—may be used socially and politically for categorizing people (e.g. “white”, “black”, “Hispanic”) but does not actually align with “pure” or discrete groups. The authors of the statement note:

“The groupings of people that exist in our species are socially-defined, dynamic, and continually evolving — amalgamations of socially- and biologically-interacting individuals with constantly-shifting boundaries, reflecting the myriad ways that individuals, families, and other clusters of people create ties, move, trade, mate, reproduce, and shift their social identities and affiliations through time. Race does not capture these histories or the patterns of human biological variation that have emerged as a result. Nor does it provide a clear picture of genetic ancestry.”

So while people think they're using biology to classify people into races, the traits that we typically consider are arbitrary and socially informed and the patterns in those traits don't map onto racial groups the way people think they do.

Tina Lasisi, a Ph.D. student at Penn State University who helped write the statement, sums it up this way “We aren't denying that patterns of genetic variation exist, in fact that's precisely what most of us study. We are however saying that race is not a useful framework for discussing or investigating human biological variation and continuing to use it stalls science more than it advances it.”

Professor Ewan Birney, Director of EMBL’s European Bioinformatics Institute, who was not involved with writing this statement, commented to me that “It is sadly all too easy to think race is somehow the everyday manifestation of human genetics but the truth is far more complex and interesting. Our collective genetic history is messier, richer and more complex than concepts of race race itself is more a cultural phenomenon and less genetics than most people realize.”

Race is real

Another important point that this statement raised is that “while human racial groups are not biological categories, ‘race’ as a social reality — as a way of structuring societies and experiencing the world — is very real. Dr. Adam Rutherford, another geneticist and author who was not involved in writing this statement, agrees with this point.

“It isn’t good enough to say that race doesn’t exist, tempting though that might be. Race certainly does exist, because we perceive it and racism exists because we enact it. What is unequivocal is that the colloquial and traditional descriptions of race that are commonly used in the West are not accurately reflected by underlying genetics. Much of this disconnect is derived from the historical roots of the pseudoscience of race, founded in the so-called Age of Enlightenment, by writers and thinkers, most of whom did not visit the continents or the people they were attempting to categorize. These clumsy, erroneous and judgmental taxonomies stuck and echo into the present.”

Ancestry testing and race

As I have already discussed in the first post of my series on direct to consumer genetic testing, most people’s understanding of what our genomes can tell us is often influenced by the claims of commercial ancestry companies to “tell you who you are.” And while many of these companies are holding special sales on their tests to commemorate DNA Day, it’s worth noting the AAPA’s caution that these oversimplified claims can reinforce concepts of race as discrete genetic categories:

“Genetic ancestry tests can identify clusters of individuals based on patterns of genetic similarity and difference, but the particular clusters we infer depend on the individuals included in the analysis. Genetic ancestry tests also tend to equate present-day peoples and contemporary patterns of genetic variation with those that existed in the past, even though they are not identical. In this regard, ancestry tests often oversimplify and misrepresent the history and pattern of human genetic variation, and do so in ways that suggest more congruence between genetic patterns and culturally-defined categories than really exists.”

There are many ways to celebrate DNA today, including reading the original paper (it’s only a page long) , extracting DNA with your kids at home , reading award-winning essays submitted to the American Society of Human Genetics by students, or browsing the #DNADay19 hashtag on twitter to see gleeful and geeky tweets by scientists. Thanks to the AAPA, you can now add to your list of activities “learn about genetics and race.” As Professor Agustín Fuentes (University of Notre Dame), one of the co-authors, encourages: “This statement reflects the reality of what we know from the science of race and racism. At this point ignorance is unacceptable. We hope people read it, use it and build from it."


Why does DNA replication need to occur?

DNA is like the instruction manual for building and operating a cell.

Explanation:

DNA replication needs to occur because existing cells divide to produce new cells.

Each cell needs a full instruction manual to operate properly. So the DNA needs to be copied before cell division so that each new cell receives a full set of instructions!

Here is a video which uses an animated tutorial to explain the process of DNA replication.

Primarily for cell division

Explanation:

Basically, every time a cell undergoes mitosis (one kind of cell division), various enzymes work to split each DNA strand in half, and then replace the missing half on the separated strands with corresponding nucleotides, leaving you with two identical strands. When the entirety of a cell's genome is copied (along with all the organelles), the cell can split into two daughter cells.
Imagine slicing yourself down the middle and splitting yourself in half, and then using each half of you as a template to recreate the other half.
That's the biology behind it, but the bottom line is that DNA is replicated in order to reproduce itself.