Gene regulation: more to muscle than MyoD

Article Abstract:

One of the deeper and more challenging questions in modern biology is the enigma of differentiation. All humans begin as a single cell, and yet after a few divisions, cells begin to become different, that is, differentiate, into muscle cells, brain cells, blood cells, and all the other cell types of the body. Why the presumably genetically identical daughter cells diverge on their path of development is thought to result from slight differences in a cell's environment that turn different genes on and off, resulting in a new genetic 'program'. Several years ago, the single gene MyoD was thought to be the master switch that began the sequence of cellular differentiation into muscle. This was demonstrated by the introduction of MyoD into mouse fibroblasts, a cell type generally involved in connective tissue and wound healing. After the fibroblasts were transfected with the MyoD gene, they differentiated as muscle cells. As fascinating as this evidence was, new evidence is accumulating that the differentiation of muscle cells is likely to be more complicated than simply turning on the MyoD gene. The first evidence was that MyoD is actually only the gene for one of a set of at least four closely related proteins, all of which play a central role in muscle differentiation. Furthermore, these proteins seem to play different roles at different times during muscle cell development. Now, in a report in the March 29, 1990 issue of Nature, researchers have reported new evidence that more is going on in muscle differentiation than simply the activation of MyoD. The researchers have shown that when the MyoD gene is introduced into liver cells, muscle differentiation does not occur. However, if these liver cells are then fused with fibroblasts, muscle differentiation proceeds. Their conclusion is that the effect of MyoD is dependent on other as yet unidentified factors. These factors apparently inhibit the action of MyoD in the liver cells, but permit it in the fibroblasts. The events that lead to the differentiation of progenitor cells into muscle cells are apparently more complex than originally suggested by MyoD research, and these events will probably continue to remain elusive for some time to come. (Consumer Summary produced by Reliance Medical Information, Inc.)

Genetic aspects, Muscles, Embryology, Animal embryology, Myogenesis, editorial

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False start on manic depression

Article Abstract:

While genetics research as a whole is making good progress, there has been a setback in the understanding of genetic predisposition to psychiatric disease. In 1987, scientists reported they had discovered a genetic marker for manic depression, an illness in which patients alternate between periods of extreme excitement, known as mania, and depression. It now appears that the connection was actually a coincidence. The original research was conducted in the Amish community, which offered several advantages for the study of genetic traits. The Amish tend to have large families, whose members stay in the community for life. They avoid habits such as drinking and drug use that might contribute to illness and confound the influence of genetics. Most importantly, the Amish are more inbred than other groups in society, so that an abnormal gene is likely to show up consistently in all affected relatives. Given these relatively optimal research conditions, investigators were encouraged when they found two marker genes that had consistent variations in persons disposed to manic depression within a large Amish pedigree. The marker genes were not thought to be responsible for manic depression, but rather to mark the area on a chromosome near the elusive gene causing the illness; researchers would then focus on this area to try to isolate the gene that actually causes the disease. But the connection was shaken when two members of this same line of descent developed manic depression and did not have the genetic markers. Other developments also suggested that the proposed connection was due to chance. Experts still believe that there is an inherited predisposition to develop psychiatric diseases such as schizophrenia and manic depression, and that researchers will eventually isolate the genes involved; this false start simply suggests that the discovery process will be more difficult than they hoped. A combination of several genetic mutations may cooperate in determining susceptibility to psychiatric disease, as appears to be true for inheritance of coronary artery disease.

Health aspects, Causes of, Depression, Mental, Depression (Mood disorder), Genetic disorders, Bipolar disorder, Amish, Heredity, Human, Human heredity

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The new biology of immune recognition

Article Abstract:

At the conference 'New Horizons in Immunology', which met during the week of November 15, 1990, the latest developments in the understanding of the process of recognition of foreign molecules by cells of the immune system was reported. Major histocompatibility (MHC) antigens are a group of molecules used by the body to recognize a molecule as foreign. If recognition is made, the MHC molecules form a complex with these molecules. This complex is then recognized by T lymphocytes and an immune reaction can be initiated. Recent research has revealed how a portion of the foreign molecule associates with the MHC molecule. Additional research involves the regulation of the immune response. If certain molecules form complexes with MHC molecules, they are considered foreign and an immune response is elicited. However, for other molecules, the immune response is not initiated. When this control of 'nonresponsiveness' is not working properly, autoimmune disease can occur. Autoimmune disease is when an immune response occurs against normal body components that should not be recognized as foreign. Scientists are trying to understand why an autoimmune response occurs, the genetic changes that are responsible, and possible ways to prevent this reaction. The role of the immune response in the development of immunodeficiency diseases, such as AIDS, was discussed, along with the design of vaccines that would neutralize or suppress the immune response, rather than stimulate the immune system. The role of the immune response in allergic reactions, such as asthma, was also discussed. (Consumer Summary produced by Reliance Medical Information, Inc.)

Allergy, Autoimmune diseases, Immune response, Immunodeficiency

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