Answered: How could one use the Agrobacterium…

How could one use the Agrobacterium tumefaciens method to introduce scent (as from a rose) into a scentless flower (such as myositis, aka "forget me not") utilizing the RhNUDX1 gene?

Principles Of Radiographic Imaging: An Art And A Science

6th Edition

ISBN:9781337711067

Author:Richard R. Carlton, Arlene M. Adler, Vesna Balac

Publisher:Richard R. Carlton, Arlene M. Adler, Vesna Balac

Chapter41: Radiation Therapy

Section: Chapter Questions

Problem 8RQ

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What is the role of Agrobacterium tumefaciens in the production of transgenic plants? a. Genes from A. fume fociens are inserted into plant DNA to give the plant different traits. b. Transgenic plants have been given resistance to the pest A. tumefacaens. c. A. wmefaciens is used as a vector to move genes into plant cells. d. Plant genes are incorporated into the genome of Agrobacterium tumefaciens.
There have been recurring cases of mad-cow disease in the United Kingdom since the mid-1990s. Mad-cow disease is caused by a prion, an infectious particle that consists only of protein. In 1986, the media began reporting that cows all over England were dying from a mysterious disease. Initially, there was little interest in determining whether humans could be affected. For 10 years, the British government maintained that this unusual disease could not be transmitted to humans. However, in March 1996, the government did an about-face and announced that bovine spongiform encephalopathy (BSE), commonly known as mad-cow disease, can be transmitted to humans, where it is known as variant Creutzfeldt-Jakob disease (vCJD). As in cows, this disease eats away at the nervous system, destroying the brain and essentially turning it into a spongelike structure filled with holes. Victims experience dementia; confusion; loss of speech, sight, and hearing; convulsions; coma; and finally death. Prion diseases are always fatal, and there is no treatment. Precautionary measures taken in Britain to prevent this disease in humans may have begun too late. Many of the victims contracted it over a decade earlier, when the BSE epidemic began, and the incubation period is long (vCJD has an incubation period of 10 to 40 years). A recent study concluded that 1 in 2,000 people in Great Britain carry the abnormally folded protein that causes vCJD. In spite of these numbers, the death rate from vCJD remains low. It is not clear whether this means that the incubation period for the disease is much longer than previously thought, or whether they may never develop the disease. What measures have been taken to stop BSE?
There have been recurring cases of mad-cow disease in the United Kingdom since the mid-1990s. Mad-cow disease is caused by a prion, an infectious particle that consists only of protein. In 1986, the media began reporting that cows all over England were dying from a mysterious disease. Initially, there was little interest in determining whether humans could be affected. For 10 years, the British government maintained that this unusual disease could not be transmitted to humans. However, in March 1996, the government did an about-face and announced that bovine spongiform encephalopathy (BSE), commonly known as mad-cow disease, can be transmitted to humans, where it is known as variant Creutzfeldt-Jakob disease (vCJD). As in cows, this disease eats away at the nervous system, destroying the brain and essentially turning it into a spongelike structure filled with holes. Victims experience dementia; confusion; loss of speech, sight, and hearing; convulsions; coma; and finally death. Prion diseases are always fatal, and there is no treatment. Precautionary measures taken in Britain to prevent this disease in humans may have begun too late. Many of the victims contracted it over a decade earlier, when the BSE epidemic began, and the incubation period is long (vCJD has an incubation period of 10 to 40 years). A recent study concluded that 1 in 2,000 people in Great Britain carry the abnormally folded protein that causes vCJD. In spite of these numbers, the death rate from vCJD remains low. It is not clear whether this means that the incubation period for the disease is much longer than previously thought, or whether they may never develop the disease. If you were traveling in Europe, would you eat beef? Give sound reasons why or why not.
Figure 9.17 Which of the following statements about quorum sensing is false? Autoinducer must bind to receptor to turn on transcription of genes responsible for the production of more autoinducer. The receptor stays in the bacterial cell but the autoinducer diffuses out. Autoinducer can only act on a different cell: it cannot act on the cell in which it is made. Autoinducer turns on genes that enable the bacteria to form a biofilm.
Which of these statements is true? An antibiotic is any substance produced by a organism that is antagonistic to the growth of prokaryotes An antibiotic is any substance produced by a prokaryote that is antagonistic to the growth of other viruses An antibiotic is any substance produced by a prokaryote that is antagonistic to the growth of eukaryotic cells An antibiotic is any substance produced by a prokaryote that prevents growth of the same prokaryote.
Arrange the following list into the correct sequence for part of the cycle of a retrovirus: 1. dsDNA integrated into host DNA 2.viral proteins synthesized on host ribosomes 3. viral DNA uses host enzymes to transcribe viral RNA 4. reverse transcriptase catalyzes synthesis of ssDNA 5. synthesis of second DNA strand (a) 5, 2, 1, 3, 4 (b) 5, 2, 3, 4, 1 (c) 4, 5, 1, 3, 2 (d) 4, 1, 2, 3, 5 (e) 2, 1, 3, 4, 5
Figure 21.10 Which of the following statements is false? In the lytic cycle, new phages are produced and released into the environment. In the lysogenic cycle, phage DNA is incorporated into the host genome. An environmental stressor can cause the phage to initiate the lysogenic cycle. Cell lysis only occurs in the lytic cycle.
There have been recurring cases of mad-cow disease in the United Kingdom since the mid-1990s. Mad-cow disease is caused by a prion, an infectious particle that consists only of protein. In 1986, the media began reporting that cows all over England were dying from a mysterious disease. Initially, there was little interest in determining whether humans could be affected. For 10 years, the British government maintained that this unusual disease could not be transmitted to humans. However, in March 1996, the government did an about-face and announced that bovine spongiform encephalopathy (BSE), commonly known as mad-cow disease, can be transmitted to humans, where it is known as variant Creutzfeldt-Jakob disease (VCJD). As in cows, this disease eats away at the nervous system, destroying the brain and essentially turning it into a spongelike structure filled with holes. Victims experience dementia; confusion; loss of speech, sight, and hearing; convulsions; coma; and finally death. Prion diseases are always fatal, and there is no treatment. Precautionary measures taken in Britain to prevent this disease in humans may have begun too late. Many of the victims contracted it over a decade earlier, when the BSE epidemic began, and the incubation period is long (VCJD has an incubation period of 10 to 40 years). A recent study concluded that 1 in 2,000 people in Great Britain carry the abnormally folded protein that causes VCJD. In spite of these numbers, the death rate from VCJD remains low. It is not clear whether this means that the incubation period for the disease is much longer than previously thought, or whether they may never develop the disease. How can a prion replicate itself without genetic material?
What is the evidence that the metamonads, which lack mitochondria, derive from ancestors that had mitochondria rather than from ancestors that were in lineages that never contained mitochondria?
The prospect of using gene therapy to alleviate genetic conditions is still a vision of the future. Gene therapy for adenosine deaminase deficiency has proved to be quite promising, but many obstacles remain to be overcome. Currently, the correction of human genetic defects is done using retroviruses as vectors. For this purpose, viral genes are removed from the retroviral genome, creating a vector capable of transferring human structural genes into sites on human chromosomes within target-tissue cells. Do you see any potential problems with inserting pieces of a retroviral genome into humans? If so, are there ways to combat or prevent these problems?