Essay 72 Stem Cells

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Stem cells are cells that grow and divide without limitation and, given the proper signals, can become any other type of cell.

Some stem cells are embryonic in origin. As a human embryo grows, the early cells start dividing and forming different, specialized cells such as heart cells, bone cells, and muscle cells. Once formed, specialized nonstem cells can only divide to produce replicas of themselves. They cannot backtrack and become a different type of cell.

Embryonic stem cells retain the ability to become virtually any cell type (Figure E7.2). If the cells are harvested from an early embryo (about 5-7 days after conception) and nudged in a particular direction in the laboratory, they can be directed to become a particular tissue or organ.

Tissues and organs grown from stem cells in the laboratory may some day be used to replace organs damaged in accidents or organs that are gradually failing due to degenerative diseases. Degenerative diseases start with the slow breakdown of an organ and progress to organ failure. Additionally, when one organ is not working properly, other organs are also affected. Degenerative diseases include stroke, diabetes, liver and lung diseases, heart disease, and Alzheimer's disease.

Stem cells could provide healthy tissue to replace those damaged by spinal cord injury or burns. New heart muscle could be produced to replace that damaged dur-

Figure E7.2 Early human embryos in a petri dish.

ing a heart attack. A diabetic could have a new pancreas, and people suffering from osteoarthritis could have replacement cartilage to cushion their joints. Thousands of people waiting for organ transplants might be saved if new organs were grown in the lab.

One problem with stem-cell research is that the embryos are destroyed when the stem cells are removed— and many people object to the destruction of early embryos. Currently, the federal government will fund research using leftover embryos from fertility treatments, but will not support research using embryos created solely for research purposes. This ban only applies to federally funded research projects, which means that in the United States, research on embryos can only be performed by genetic engineers who obtain grants from nongovernmental sources unless they have access to the limited numbers of embryos created during fertility treatments.

In vitro (Latin, meaning "in glass") fertilization procedures often result in the production of excess embryos because a large number of egg cells are harvested from a woman who wishes to become pregnant. These egg cells are then mixed with her partner's sperm in a petri dish, resulting in the production of many fertilized eggs that grow into embryos. A few of the embryos are then implanted into the woman's uterus. The remaining embryos are stored so that more attempts can be made if pregnancy does not result or if the couple desires more children. When the couple achieves the desired number of pregnancies, the remaining embryos can, with the couple's consent, be used for stem-cell research.

A solution to the ethical dilemma presented by the use of embryonic stem cells seems to be on the horizon. Scientists have recently discovered that many adult tissues also contain stem cells. Recent studies published in peer-reviewed literature suggest that most adult tissues have stem cells, that these cells can be driven to become other cell types, and that they can be grown indefinitely in the laboratory. Based on success in animal models, there is even evidence that adult stem cells will help cure diseases. In fact, scientists have used stem cells from adult tissues to repair damage in animals due to heart attack, stroke, diabetes, and spinal cord injury.

defective gene in SCID patients. After the immune-system cells are infected with the virus, these recombinant cells, which now bear copies of the functional gene, are returned to the SCID patient (Figure 7.20a).

In 1990, a four-year-old girl named Ashi DiSilva (Figure 7.20b) was the first patient to receive gene therapy for SCID. Ashi's parents were willing to face the unknown risks to their daughter because they were already far too familiar with the risks of SCID—the couple's two other children also had SCID and were severely disabled. Ashi is now a healthy adult with an immune system that is able to fight off most infections.

1. Remove immune-system cells from patient.

2. Infect the cells with a 3. Return cells carrying virus carrying the normal the normal allele.

allele.

Figure 7.20 Gene therapy in an SCID patient. (a) A virus carrying the normal gene is allowed to infect immune-system cells that have been removed from a person with SCID. The virus inserts the normal copy of the gene into some of the cells, and these cells are then injected into the SCID patient. (b) Ashi DiSilva, the first gene therapy patient.

1. Remove immune-system cells from patient.

2. Infect the cells with a 3. Return cells carrying virus carrying the normal the normal allele.

allele.

Figure 7.20 Gene therapy in an SCID patient. (a) A virus carrying the normal gene is allowed to infect immune-system cells that have been removed from a person with SCID. The virus inserts the normal copy of the gene into some of the cells, and these cells are then injected into the SCID patient. (b) Ashi DiSilva, the first gene therapy patient.

However, Ashi must continue to receive treatments, because blood cells, whether genetically engineered or not, have limited life spans. When most of Ashi's engineered blood cells have broken down, she must be treated again. Thus, she undergoes this gene therapy a few times each year. Since Ashi's treatment, many other SCID patients have been successfully treated and live normal lives. Unfortunately, Ashi's gene therapy does not prevent her from passing on the defective allele to her biological children because this therapy is not "fixing" the allele in her ovaries.

Even though Ashi will need lifelong treatment and could pass the defective allele to her children, she is lucky that her genetic disease was amenable to gene therapy. There are not many genetic diseases for which the defective cells can be removed from the body, treated, and reintroduced to the body. Nor are there many genetic diseases for which contributions from many genes and the environment are not a factor.

For gene therapy to be successful in curing more genetic diseases, it is necessary for scientists to not only deliver the gene to the correct location, they must also make sure the gene is turned off and on at the proper times. In other words, the expression of the gene must be regulated.

Regulating Gene Expression Scientists will only succeed with gene therapy if they can learn to regulate the expression of a gene once it is located in the proper place. Recall from Chapter 4 that each cell in your body, except sperm or egg cells, has the same complement of genes you inherited from your parents. However, different genes are expressed in different cells at different times. Heart cells differ from eye cells because each cell type expresses only a small percentage of its genes. For gene therapy to work, scientists must learn how to turn the right genes on in the right cell type at the right time.

With rBGH, farmers can regulate how much protein to inject into the bloodstream of a cow, but a gene inserted into the genome must respond to environmental cues telling it when and when not to produce a protein.

Gene expression is most commonly regulated—turned off or on modulated more subtly—by controlling the rate of transcription. Adjacent to an actual gene is a sequence of nucleotides called the promoter, which functions in helping to

Various proteins activate or repress the rate of polymerase binding to the promoter, affecting the rate of transcription.

Various proteins activate or repress the rate of polymerase binding to the promoter, affecting the rate of transcription.

RNA polymerase enzyme must bind to Gene of interest the promoter region before transcription of the gene can begin.

Figure 7.21 Regulation of gene expression. When a gene needs to produce the protein it encodes, the RNA polymerase enzyme binds to the promoter adjacent to the gene to begin transcription. Other proteins, called activators or repressors, increase or decrease the rate of polymerase binding, thereby influencing the overall rate of protein synthesis.

RNA polymerase enzyme must bind to Gene of interest the promoter region before transcription of the gene can begin.

Figure 7.21 Regulation of gene expression. When a gene needs to produce the protein it encodes, the RNA polymerase enzyme binds to the promoter adjacent to the gene to begin transcription. Other proteins, called activators or repressors, increase or decrease the rate of polymerase binding, thereby influencing the overall rate of protein synthesis.

Media Activity 7.1B Regulation of gene expression regulate gene expression. When a cell requires a particular protein, the RNA polymerase enzyme binds to the promoter for that particular gene and transcribes the gene. Other proteins in the cell can activate or repress the rate at which the polymerase binds to initiate transcription as well (Figure 7.21).

The rate at which the polymerase binds to the promoter is also affected by substances that are present in the cell. For example, the presence of alcohol in a liver cell might result in increased transcription of a gene involved in the breakdown of alcohol.

Once genetic engineers find better methods for delivering gene sequences to the required locations and can regulate their expression, gene therapy will be far more effective. However, gene therapy is an attempt to modify only one or a few genes. A far more controversial type of genetic engineering involves making an exact copy of an entire organism, a process called cloning.

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