2. How can one gene code for more than one kind of polypeptide (protein)?
a. by recombinant DNA
b. with use of plasmids
c. by making alternative forms of RNA
d. all of the above

3. How can scientists get more DNA for analysis from a small sample at a crime scene?
a. STR
b. RFLP
c. PCR
d. it is not possible

4. What is true of the development of pesticide resistance in an insect population?
a. spraying the pesticide created the mutation that led to resistance
b. the resistance gene must have been in some members of the population before the spraying
c. natural selection created the gene for resistance
I forgot to add another choice for question 4.
d. it is not possible

Can someone help me with this biology questions? is a post from: Nature Technology Corporation

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I need to modify it appropriately so that you can isolate and define a minimal E.coli promoter.

I am specifically interested in knowing about the selection scheme, modifications of the vector platform if necessary, any reporter gene assays etc – so please highlight these in your approach and provide me with a rationale for any alterations from the initial method. Thank you!
instead of lacz can you uase a temperature sensitive mutant?

How can you isolate and define a minimal E. coli promoter? is a post from: Nature Technology Corporation

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In the colorful life of the world, what causes the diversity of life creating attractive? After years of painstaking research professor at Nanjing University boldly made “Indel mutation hypothesis”, with the newly discovered “universal mechanism of genetic mutation,” cracked the biology of many suspense. July 20, the latest issue of “Nature” magazine published in Nanjing University to complete this independent research.

In the “natural” “published in eukaryotes insertion / deletion mutations increase the rate of the surrounding sequences,” the paper, College of Life Science, Nanjing University, Professor Tian Dacheng, Chen and other independent groups and several drafts to complete wisdom.

Since 2005, their bio-informatics technology by human, chimpanzee, rhesus monkeys, mice, fruit flies, such as rice and different types of yeast genome sequences were compared to the analysis. Research found, DNA insertion / deletion (Indel) will cause a series of variations around. On this basis, they proposed “Indel mechanism of spontaneous mutation induction hypothesis”, the success from the source to answer the “how the genetic variation of the formation of” the fundamental problems facing the life sciences. The hypothesis that the genome of different species can be used for reference frame to be tested, and received the support of a variety of test results.

Tian Dacheng explained that the mutations mainly refers to the nucleotide sequence of DNA, type and amount of change, and DNA sequence common point (bp) mutation is the basic source of genetic variation. Point mutations are divided into spontaneous mutation and induced mutation. For a long time, the academic system of the classical understanding of spontaneous mutation is spontaneous mutations by a number of factors, the result is a series of changes, with the randomness and rarity. But as the last century since the 90′s DNA sequencing technology breakthrough, the researchers of the spontaneous mutations in the genome with the number and distribution of accurate estimates, and generally considered the “spontaneous mutations in the genome are not randomly distributed, the mutation Hot widespread in the genome. ” This conclusion of the spontaneous mutation of traditional understanding of randomness and rarity, tremendous challenge, and this phenomenon has caused great concern among scientists, but unfortunately has not found a general mechanism to explain this major scientific questions.

Tian Dacheng and other genetic mutations discovered a new mechanism is of great scientific significance, successfully cracked a lot of suspense on biological genetics: first, all regions of the genome mutation rate is very different, the number of spontaneous mutation is the number and density of the Indel decision, the number of spontaneous mutations are not rare in Indel near, far away from Indel region is rare, but Indel itself is a point mutation, its occurrence has some randomness, so the induced mutations also have a certain randomness; Second, find the source of the majority of spontaneous mutation, ie, biological diversity, the initial source of variation is mainly induced by the Indel; Third, natural selection to a large extent by the choice of the Indel implementation The level of spontaneous mutation rate is largely the result of natural selection; Fourth, biological variation through the ability to regulate their own ability to adapt to the environment than people originally expected, though, that the role of mutations in evolution enormous .

The results not only lead to a large number of scientific issues, also has potential applications, such as the somatic cells of the Indel mutation effects may be the key to unlock the mechanism of tumor; large Indel overall mutation effects, understanding the origin of life play an important role; Indel amplification mutation heterozygote effect, the mutation rate can significantly increase the genetic breeding of crops have significant potential value.

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Chinese scientists have found genetic mutation common mechanism is a post from: Nature Technology Corporation

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Canadian scientists have identified a gene that makes some people susceptible to major depressive disorders. Speaking at the Forum of European Neuroscience today (9 July), Professor Nicholas Barden explained, “This is a major breakthrough in the realm of psychiatry and will have groundbreaking implications for diagnosis and the development of new anti-depressant treatment.”

It has been known for many years that genetic factors are at the base of depression and bipolar disorder, but the complex molecular networks involved remain unknown. “The actual gene, known as P2RX7, is found in humans and animals and is responsible for depression. It has taken many years to find,” said neuroscientist, Professor Barden from CHUL Research Centre in Quebec. Finding it is highly significant in uncovering the molecular pathways involved in depression. The results were published in May 2006 American Journal of Medical Genetics*

During their lifetime, about 5-12% of men and 10-25% of women will experience at least one episode of major depression. People with bipolar disorder – also known as manic depression – experience extreme mood swings. The total social cost of depressive disorders is estimated to be billions of dollars per year. By 2020, depression is expected to rank first in disease burden in economically developed countries.

Depression has until now often been associated with the serotonin system in the brain, a system that can influence mood and emotion. “What is particularly exciting is that P2RX7 has nothing to do with serotonin,” said Professor Barden. Drugs that boost the flow of serotonin can be effective anti-depressants, but take weeks to take effect. The fact that P2RX7 that has nothing to do with serotonin could partly explain why.

Animal studies have shown that this gene is expressed in brain areas known to be involved in depression, and depressive-like behaviour in mice could be reversed by treatment with drugs that stimulate P2RX7.

P2RX7 also plays an important role in the brain’s response to inflammation, which is known to be part of many neuropsychiatric disorders. Additionally, stress hormones decrease the activity of this gene, suggesting a mechanism for the onset of depression following severe stress.

“A person may have the mutated gene, but its ‘default setting’ means that they may not develop depression. We don’t yet know how P2RX7 works and we still believe that a multitude of genes feed into the same pathway that may induce depression,” said Professor Barden.

The identification of the gene means that anti-depressants in the future could target the gene directly. With anti-depressants currently targeting the serotonin system, P2RX7 is bypassed to an extent. In animal studies, activators of P2RX7 have an immediate anti-depressant action, giving hope that new anti-depressant medication, with a new mechanism of action, can be developed.

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Canadian Scientists Discover Gene for Depression is a post from: Nature Technology Corporation

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THE genome of the cucumber has been sequenced by an international consortium lead by Chinese and U.S. institutions. The annotated genome was published online November 1 by the journal Nature Genetics.

The cucumber genome will give insight into the genetics of the whole cucurbit family, which includes pumpkins and squash, melon and watermelon, and be a platform for research in plant biology, said William Lucas, professor and chair of the Department of Plant Biology at the University of California, Davis. Lucas helped with the development and management of the project.

“This is going to help a large community, we can now go ten times faster than we could before,” Lucas said.

Lucas studies the vascular transport systems, phloem and xylem, that plants use to move nutrients, minerals and signaling molecules throughout the body of the plant. Pumpkins and cucumber are model plants for studying vascular transport, because their vascular system is large and easy to access.

The Lucas research group has shown that plants use both proteins and RNA Ð molecules copied or transcribed from DNA, as signaling molecules that are transported around the plant through the phloem. These signals can affect plant growth, coordinate activity through the plant and help it fight infection. For example, in 2007 they showed that “florigen,” the signal that tells the growing tips of plants to make flowers in response to seasonal changes, is a protein transmitted through the phloem.

The new study identified 800 phloem proteins in the cucumber genome. With the help of the genome data, researchers will be able to rapidly identify and characterise all the protein, RNA and other molecules in the phloem sap, Lucas said.

There are already indications that far more is going on in the phloem than anybody, “including me,” had previously expected, he said.

The study shows that five of the seven chromosomes in cucumber arose from ten ancestral chromosomes shared with melon, and gene-coding stretches of DNA share about 95 per cent similarity to melon. Preliminary studies in the Lucas lab at UC Davis have established comparable similarity between cucumber and pumpkin.

The cucumber genome will also provide insights into traits such as disease and pest-resistance, the “fresh green” odour of the fruit, bitter flavors and sex expression.

The cucumber is the seventh plant to have its genome sequence published, following the well-studied model plant Arabidopsis thaliana, the poplar tree, grapevine, papaya, and the crops rice and sorghum.

The sequencing effort, begun earlier this year, was coordinated by Professor Sanwen Huang of the Chinese Academy of Agricultural Science and included the Genome Center at the Beijing Genome Institute-Shenzhen and UC Davis as well as several laboratories in China and others in the U.S., Denmark, the Netherlands, Australia and South Korea.

Part of the effort relied on new methods developed by the Beijing Genome Institute to assemble short pieces of DNA, about 50 base pairs, into the sequence. The Beijing Genome Institute-Shenzhen can now sequence and assemble genomes much faster, and at lower cost, than previously possible, Lucas said.

“This will be the forerunner for many genomes done at a cost-effective rate,” he said.

Scientists sequence genome of cucumber is a post from: Nature Technology Corporation

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The other 2 doctors–Doctors Sagan & Kaprowski–were had immigrated from Russia & Germany after being hired by the U.S. government to come up with solutions, as they were one of the more prominent names in medicine at the time.

The prize to who ever came up with a vaccine for polio was enormous, along with getting fame they would receive boat loads of me, and with that in mind, the 2 doctors began a competition to see who would come up with a cure first. Now, to find a cure for polio, both doctors needed to test the effects various medicines would have on people, they could not do this in the U.S. fore 2 reasons;

1) It was illegal to use humans as guinea pigs for lab experiments (atleast if they were white)

2) Dr. Salk had already immunized large portions of the American population

So the 2 doctors decided to go outside America to test their vaccines. Dr. Sagan went to Russia, and Dr. Kaprowski went to Africa.

Long story short, Dr. Sagan’s vaccine proved effective in immunizing the children of some Easern European countries–Latvia, Estonia, etc., and it became the vaccine that we use today to treat it

____________________________________________

Dr. Kaprowski , on the other hand, in creating his vaccine, was careless about the methods he used. Part of his soluition involved using chimp DNA and incorporating it into his medicine, unfortunately for him (and eventually for about 70% of Africa) his solution was infected with the chimp equivalent of what we now know as HIV/AID’s, but Dr. Kaprowski could care less about making sure ke didn’t kill the patients he tested on —he was seeking money, fame, & glory.

So, with the help of the U.S. government , & the WHO he administered a virus (which he told the citizens of Burundi, Rwanda, & the Congo) was a vaccine for polio, to 1,000, 000 people.

The rest is history, the AID’s virus spread like wild fire throughout those regions, and eventually into other surrounding countries as well.

Now, there are alternate theories that suggest that a man had either fornicated with a monkey, cut himself while cleaning a monkey, or been bitten by a monkey and that is how the various came about. What this theory fails to explain is why the AID’s virus never developed until polio vaccinations were given by American doctors to Africans, since humans have hunted & eaten monkeys (chimps) for hundreds (if not thousands) of years. Today the epicenter of the disease is in those regions where Dr. Kaprowski administered his vaccinations to Africans, and today–50 years later–70% of the continent has the terminal illness, and 100, 000, 000 children are expected to die from it by the end of the century
The origin of aids:

Controversial discussions on AID’s:

What do you think about this documentary (summarized) regarding the origins of AID's/HIV? is a post from: Nature Technology Corporation

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http://www.expoherbs.com

Experts say a lack of funds is slowing attempts to find a truly effective vaccine against genital herpes, a sexually transmitted disease that can be devastating for the one in five Americans over 12 who carry the virus.

Genital infection with the herpes simplex viruses (HSV) 1 or 2 is not just an inconvenience, doctors note. It is a painful, recurrent illness that causes psychological distress, raises health risks for newborns, and boosts the carrier’s odds for a much more deadly virus, HIV.

And even as the Herpevac trial — the first major publicly funded trial of a preventive vaccine — is set to get under way, a leader of that trial says the vaccine, even if successful, would not be the solution to the herpes epidemic.

“The Herpevac trial is a vaccine that is only going to affect the [uninfected] adolescent woman,” said Dr. Lawrence Corey, head of infectious diseases and virology at the University of Washington, in Seattle. “It is not going to be effective in men or in those who are HIV-positive. We need to do better.”

Prior, expensive failures have made the drug industry skittish about funding herpes vaccine trials, however. So, despite the fact that most adult Americans either have HSV-1 or 2, or are at very high risk of contracting it in their lifetime, not enough is being done to stop the pathogen.

“I would say that, at the moment, the genital herpes vaccine is a field that does not have much interest, does not have much money,” Corey said. “The need for an HSV vaccine is really substantive, but there is not much of a program in the industrialized, developing world to develop such a vaccine.”

Part of the problem lies in the complexity of the virus. While simpler viruses such as the flu simply mutate their outer coats to evade the human immune system, HSV and other persistent viral infections are much more stable.

However, they have another secret weapon. Compared to other viruses, HSV 1 and 2 “have a lot more genes and gene products that are redirecting and subverting the [host] immune response,” Corey explained.

Although the two strains are similar and can infect either mouth or genitalia, HSV-1 is the prime cause of oral herpes (cold sores and fever blisters), while HSV-2 is the usual source of genital infections.

Another tactic keeps herpes well-shielded from immune attack. Unlike pathogens that spread in readily accessed blood, HSV hides out in nerve cells called dorsal ganglia, located in the back. Specific triggers, such as sun exposure or stress, can send the virus traveling through nerve pathways to mucosal sites of activity in the genitalia, mouth and even eyes.

These nerve cells are “a protected site, immunologically,” explained Dr. Lawrence Stanberry, director of the Sealy Center for Vaccine Development at the University of Texas Medical Branch in Galveston. “Needless to say, we don’t like to have our immune system attacking our nerves,” he said, so vaccines with that kind of reach are hard to develop.

And yet, progress is being made. The Herpevac trial, funded by the U.S. National Institutes of Health and drug maker GlaxoSmithKline, is focused on a preventive vaccine aimed solely at uninfected women. Preliminary, phase III studies completed last year found the vaccine to be 73 percent effective in shielding young women from infection after exposure to HSV-2.

A 73 percent effectiveness rate may not sound all that impressive, but Stanberry — also an investigator on the Herpevac trial — said no one is expecting 100 percent immunization.

“What one hopes for with a vaccine is that you get very high rates of effectiveness and then very broad uptake of the vaccine [in the population],” he explained. “So then, if almost everyone gets immunized, then the disease simply doesn’t circulate in the population to the same extent.”

Reducing the “pool” of available virus will be vital to lowering the infection rate, researchers say, because the Herpevac shot does not protect uninfected men and cannot eliminate HSV from people who are already infected.

The Herpevac trial is currently wrapping up recruitment of 7,000 healthy, HSV-negative U.S. women between the ages of 18 and 30. Participants will receive either the vaccine or a placebo and then be followed for 18 months to see if they become infected.

Stanberry said final results from the trial should be available by 2009, and — if the vaccine proves effective — a shot might be approved by 2010.

However, like most modern vaccine trials, the Herpevac trial relies on a piece or “subunit” of HSV to prime the human immune system against incoming virus.

Another researcher is advocating the use of the live — but greatly weakened — form of the virus, instead.

The problem with the subunit approach is that its effects don’t last, said William Halford, a virologist at Montana State University, in Bozeman. “Once you deliver it into someone’s body, it’s there, but, in a few weeks, it is gone,” he said.

Live virus vaccines have a long and effective history. In fact, one of the few effective vaccines against any herpes strain — the chickenpox/shingles (herpes zoster) shot — was developed from live virus back in the 1960s.

Since that time, doctors have gotten more skittish about injecting people with a live form of the virus, however, so the subunit approach took precedence.

But Halford believes it is time to revisit the idea of a live virus herpes vaccine.

“All we really have to do is to figure out a way to take away some of the genes or proteins that the virus needs to cause actual disease,” he said. In other words, people would be infected with a very weak form of HSV, one that is sufficient to trigger a sustained immune response but too frail to trigger disease outbreaks.

Halford is specifically investigating a protein in HSV called ICP0. “If I take away the gene that codes for that protein, the virus is really weakened,” he said.

The approach is controversial, but Corey believes it could have promise. “I certainly think that the live attenuated virus is a viable approach to talk about,” he said.

Funding will be the real challenge, however, whatever the vaccine strategy. According to Corey, a series of expensive failures over the past two decades has dampened the enthusiasm of industry to invest in HSV vaccine research.

“I can give my own scenario in which we worked with [drug maker] Chiron and spent seven years and a lot of money — decapitalizing the company by 25 percent — on an antibody-based vaccine,” Corey said. “At the time, we thought it would be sufficient to work, but it didn’t.”

So, with the private sector waiting on the sidelines, public funding becomes key.

“I think there needs to be more money from the publicly funded institutions — whether they be foundations, the NIH or the National Research Council, in vaccine development,” Corey said.

“We also need to do more in defining a real path of success for a genital herpes vaccine,” he added. “Once some pathway of success becomes defined, then you’ll see the pharmaceutical companies move forward.”

http://www.expoherbs.com

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Scientists Frustrated in Search for Genital Herpes Vaccine is a post from: Nature Technology Corporation

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US scientists have mapped the complete genome of a middle-aged female cancer patient who died of acute myelogenous leukemia; they decoded 3 billion bits of her DNA and identified the genes involved in her disease, including 8 new ones.

The study was the work of a large team of scientists from the Washington University School of Medicine, St Louis, Missouri and the University of Washington, Seattle, Washington and is published in the 6th November issue of the journal Nature.

Acute myelogenous leukemia (AML) is a cancer of the bone marrow that makes new blood cells and it develops as a result of DNA mutations that accumulate as a person grows older.

AML is the most common type of leukemia and occurs mostly in adults over 60 years of age. About 13,000 new cases of AML will be diagnosed in the US this year and 8,800 people will die of it. The five year survival rate is 21 per cent, according to the American Cancer Society.

However, how and why the genes mutate in AML and how the altered DNA disrupts the biological pathways that lead to uncontrolled cell growth that eventually becomes a cancer tumor is still somewhat of a mystery to science.

Senior author of the study Dr Richard K. Wilson, who is director of Washington Universitys Genome Sequencing Center in St Louis, said:

Our work demonstrates the power of sequencing entire genomes to discover novel cancer-related mutations.

A genome-wide understanding of cancer, which is now possible with faster, less expensive DNA sequencing technology, is the foundation for developing more effective ways to diagnose and treat cancer, he added.

The investigators found 10 mutated sequences in the DNA of the patients tumor that appeared to be linked to AML. Eight of them were rare and found in genes that had not been linked with the disease before.

They also found that 9 of the mutations were in every cell of the tumor while the 10th, a mutation in the FLT3 gene, was only in some of them, suggesting this was the last mutation to develop.

Previous studies have discovered some common DNA variations that could be relevant to AML risk, but the enormous contribution of this study is that the investigators sifted throught 3 billion base pairs, the individual bits of code that constitute the fundamental building blocks of a persons genome, to find the individual mutations that contributed to the patients AML.

Basically what the investigators did was a full side by side genomic comparison of the of the patients normal cells DNA (taken from a skin sample) and her cancer cells DNA. This was done before the patient underwent cancer treatment which is known to alter DNA.

This type of detailed genomic comparison has never been done before; previous studies have just looked at cancer cells and sequenced genes known or suspected to be linked to cancer, which means key mutations, especially new ones, could be overlooked.

As lead author Dr Timothy Ley, who is a hematologist and the Alan A and Edith L Wolff Professor of Medicine at the Washington University School of Medicine, explained:

Until now, no one has sequenced a patients genome to find all the mutations that are unique to that persons disease.

We didnt know what we would find, but we felt that the answers to why this patient had AML had to be embedded in her DNA, said Ley.

Geneticist and former director of the National Human Genome Research Institute, Dr Francis Collins said that unlike previous studies that had been looking under the lamppost, the investigators on this landmark study lit up the whole street.

This achievement ushers in a new era of comprehensive understanding of the fundamental nature of cancer, and offers great promise for the development of powerful new approaches to diagnosis, prevention and treatment, said Collins.

Genetic tests carried out before this study had already established that the patient had two mutations known to be common in AML. This was one of the reasons the investigators chose to sequence her genome.

Of the 2.7 million single nucleotide variants in DNA of both normal and tumor cells, they found 98 per cent of them were the same, leaving some 60,000 to look at in more detail.

Using a mix of sophisticated software and analytical tools, some developed just for this study, the investigators then looked at the parts of the DNA that issue instructions for making proteins and found which ones in the tumor sample differed from the normal sample and discovered 10 mutations (including two already known to be involved in AML).

The 8 new mutations included three in genes that normally suppress the growth of tumor cells, one being the PTPRT tyrosine phosphatase gene, which is sometimes found mutated in colon cancer.

Another four of the 8 new genes appear to be ones that promote cancer growth, including one belonging to a family of genes that are switched on in embryonic stem cells and could be playing a role in self-renewal of cells, which is thought be an important characteristic of leukemia cells, said the researchers.

And the remaining gene from the 8 new ones may have contributed to the patients resistance to chemo because it appears to interfere with delivery of drugs into cells.

The investigators are still analyzing parts of the patients DNA that is non-coded, and may still find other mutations, said Dr Elaine Mardis, co-director of the Genome Sequencing Center at Washington University, and co-lead author of the study. But as she explained:

The role of these non-coding mutations will be more of a challenge to elucidate because we do not yet fully understand the function of this part of the genome.

Another interesting discovery in this study was that when they compared the 8 new mutations from this patient with the DNA of tumor samples from 187 other AML patients there were no matches: in other words the 8 mutations appeared to be unique to this patient. Wilson said this suggested:

There is a tremendous amount of genetic diversity in cancer, even in this one disease.

There are probably many, many ways to mutate a small number of genes to get the same result, and were only looking at the tip of the iceberg in terms of identifying the combinations of genetic mutations that can lead to AML, added Wilson.

One theory that Wilson and colleagues are working on is that the mutations happen in sequence, first one mutation occurs, this has a slight tendency toward cancer, then another one and so on, gradually accumulating lots of little tendencies toward cancer, until a final tipping point that causes the cancer cells to become more dangerous is reached, explained Ley.

Wilson, Ley and colleagues are now sequencing the genome of other AML patients and they also hope to extend their whole-genome method to investigate breast and lung cancers.

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Scientists Map Cancer Patients Complete Genome is a post from: Nature Technology Corporation

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Plasmids are useful for both bacteria and scientists because they contain
a) Ribosomal RNA genes
b) one or more antibiotic resistence genes
c) Recombinant DNA products
d) all of the above

Which of the following is an application of medical or pharmaceutical biotechnology?
a) recombinant insulin
b) DNA sequencing
c) identification of endangered species
d) diease resistant cotton

I have a lousy teacher but I need help..? is a post from: Nature Technology Corporation

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how do evolutionists explain amber and DNA inside mosquitoes of humans and dinosaurs? is a post from: Nature Technology Corporation

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