You implant an FGF10-coated bead into the anterior flank of a chicken embryo, directly below the level of the wing bud. What is the phenotype of the resulting ectopic limb? Briefly describe the expected expression domains of 1) Shh, 2) Tbx4, and 3) Tbx5 in the resulting ectopic limb bud.

You implant an FGF10-coated bead into the anterior flank of a chicken embryo, directly below the level of the wing bud. What is the phenotype of the resulting ectopic limb? Briefly describe the expected expression domains of 1) Shh, 2) Tbx4, and 3) Tbx5 in the resulting ectopic limb bud.

Basic Clinical Laboratory Techniques 6E

6th Edition

ISBN:9781133893943

Author:ESTRIDGE

Publisher:ESTRIDGE

Chapter3: Basic Hemostasis

Section3.6: D-dimers

Problem 6RQ

See similar textbooks

Similar questions

You aim to test the hypothesis that the Tbx4 and Tbx5 genes inhibit each other's expression during limb development. With access to chicken embryos and viruses capable of overexpressing Tbx4 and Tbx5, describe an experiment to investigate whether these genes suppress each other's expression in the limb buds. What results would you expect if they do repress each other? What results would you expect if they do not repress each other?
The gene controlling ABO blood type and the gene underlying nail-patella syndrome are said to show linkage. What does that mean in terms of their relative locations in the genome? What does it mean in terms of how the two traits are inherited with respect to each other?
What are the roles of cellular proto-oncogenes, and how are these roles consistent with their implication in oncogenesis?
The cystic fibrosis gene encodes a chloride channel protein necessary for normal cellular functions. Let us assume that if at least 5% normal channels are present, the affected individual has mild symptoms of cystic fibrosis. Having less than 5% normal channels produces severe symptoms. At least 50% of the channels must be expressed for the individual to be phenotypically normal. This gene has various mutant recessive alleles: Predict the percent of functional channels and severity of symptoms for the following genotypes: a. heterozygous for CF100 b. homozygous for CF100 c. heterozygous, with one copy of CF100 and one of CF3 d. heterozygous, with one copy of CF1 and one copy of CF3
Who Owns Your Genome? John Moore, an engineer working on the Alaska oil pipeline, was diagnosed in the mid-1970s with a rare and fatal form of cancer known as hairy cell leukemia. This disease causes overproduction of one type of white blood cell known as a T lymphocyte. Moore went to the UCLA Medical Center for treatment and was examined by Dr. David Golde, who recommended that Moores spleen be removed in an attempt to slow down or stop the cancer. For the next 8 years, John Moore returned to UCLA for checkups. Unknown to Moore, Dr. Golde and his research assistant applied for and received a patent on a cell line and products of that cell line derived from Moores spleen. The cell line, named Mo, produced a protein that stimulates the growth of two types of blood cells that are important in identifying and killing cancer cells. Arrangements were made with Genetics Institute, a small start-up company, and then Sandoz Pharmaceuticals, to develop the cell line and produce the growth-stimulating protein. Moore found out about the cell line and its related patents and filed suit to claim ownership of his cells and asked for a share of the profits derived from the sale of the cells or products from the cells. Eventually, the case went through three courts, and in July 1990n years after the case beganthe California Supreme Court ruled that patients such as John Moore do not have property rights over any cells or tissues removed from their bodies that are used later to develop drugs or other commercial products. This case was the first in the nation to establish a legal precedent for the commercial development and use of human tissue. The National Organ Transplant Act of 1984 prevents the sale of human organs. Current laws allow the sale of human tissues and cells but do not define ownership interests of donors. Questions originally raised in the Moore case remain largely unresolved in laws and public policy. These questions are being raised in many other cases as well. Who owns fetal and adult stem-cell lines established from donors, and who has ownership of and a commercial interest in diagnostic tests developed through cell and tissue donations by affected individuals? Who benefits from new genetic technologies based on molecules, cells, or tissues contributed by patients? Are these financial, medical, and ethical benefits being distributed fairly? What can be done to ensure that risks and benefits are distributed in an equitable manner? Gaps between technology, laws, and public policy developed with the advent of recombinant DNA technology in the 1970s, and in the intervening decades, those gaps have not been closed. These controversies are likely to continue as new developments in technology continue to outpace social consensus about their use. Should the physicians at UCLA have told Mr. Moore that his cells and its products were being commercially developed?
Who Owns Your Genome? John Moore, an engineer working on the Alaska oil pipeline, was diagnosed in the mid-1970s with a rare and fatal form of cancer known as hairy cell leukemia. This disease causes overproduction of one type of white blood cell known as a T lymphocyte. Moore went to the UCLA Medical Center for treatment and was examined by Dr. David Golde, who recommended that Moores spleen be removed in an attempt to slow down or stop the cancer. For the next 8 years, John Moore returned to UCLA for checkups. Unknown to Moore, Dr. Golde and his research assistant applied for and received a patent on a cell line and products of that cell line derived from Moores spleen. The cell line, named Mo, produced a protein that stimulates the growth of two types of blood cells that are important in identifying and killing cancer cells. Arrangements were made with Genetics Institute, a small start-up company, and then Sandoz Pharmaceuticals, to develop the cell line and produce the growth-stimulating protein. Moore found out about the cell line and its related patents and filed suit to claim ownership of his cells and asked for a share of the profits derived from the sale of the cells or products from the cells. Eventually, the case went through three courts, and in July 1990n years after the case beganthe California Supreme Court ruled that patients such as John Moore do not have property rights over any cells or tissues removed from their bodies that are used later to develop drugs or other commercial products. This case was the first in the nation to establish a legal precedent for the commercial development and use of human tissue. The National Organ Transplant Act of 1984 prevents the sale of human organs. Current laws allow the sale of human tissues and cells but do not define ownership interests of donors. Questions originally raised in the Moore case remain largely unresolved in laws and public policy. These questions are being raised in many other cases as well. Who owns fetal and adult stem-cell lines established from donors, and who has ownership of and a commercial interest in diagnostic tests developed through cell and tissue donations by affected individuals? Who benefits from new genetic technologies based on molecules, cells, or tissues contributed by patients? Are these financial, medical, and ethical benefits being distributed fairly? What can be done to ensure that risks and benefits are distributed in an equitable manner? Gaps between technology, laws, and public policy developed with the advent of recombinant DNA technology in the 1970s, and in the intervening decades, those gaps have not been closed. These controversies are likely to continue as new developments in technology continue to outpace social consensus about their use. Do you think that donors or patients who provide cells and/or tissues should retain ownership of their body parts or should share in any financial benefits that might derive from their use in research or commercial applications?
Variations in Phenotype Expression Explain how camptodactyly is an example of expressivity.
What is the difference between a proto-oncogene and a tumor-suppressor gene?
Which of the following mutations will result in cancer? a. homozygous recessive mutation in a tumor-suppressor gene coding for a nonfunctional protein b. dominant mutation in a tumor-suppressor gene in which the normal protein product is overexpressed c. homozygous recessive mutation in which there is a deletion in the coding region of a proto-oncogene, leaving it nonfunctional d. dominant mutation in a proto-oncogene in which the normal protein product is overexpressed
Name three genes whose mutations lead to an altered behavioral phenotype. Briefly describe the normal function of the mutated gene as well as the altered phenotype.
Explain the role of axis formation in development.
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?