. Neurofibromas are tumors of the skin that can arisewhen a skin cell that is originally NF1+/ NF1− losesthe NF1+ allele. This wild-type allele encodes a functional protein (called a tumor suppressor), while theNF1− allele encodes a nonfunctional protein.A patient of genotype NF1+ / NF1− has 20 independent tumors in different areas of the skin. Samplesare taken of normal, noncancerous cells from thispatient, as well as of cells from each of the 20 tumors.Extracts of these samples are analyzed by a techniquecalled gel electrophoresis that can detect variantforms of four different proteins (A, B, C, and D) allencoded by genes that lie on the same autosome asNF1. Each protein has a slow (S) and a fast (F) formthat are encoded by different alleles (for example, ASand AF). In the extract of normal tissue, slow and fastvariants of all four proteins are found. In the extractsof the tumors, 12 had only the fast variants of proteinsA and D but both the fast and slow variants of proteins B and C; 6 had only the fast variant of protein Abut both the fast and slow variants of proteins B, C,and D; and the remaining 2 tumor extracts had onlythe fast variant of protein A, only the slow variant ofprotein B, the fast and slow variants of protein C, andonly the fast variant of protein D.a. What kind of genetic event described in this chapter could cause all 20 tumors, assuming that all thetumors are produced by the same mechanism?b. Draw a genetic map describing these data, assuming that this small sample represents all the typesof tumors that could be formed by the same mechanism in this patient. Show which alleles of whichgenes lie on the two homologous chromosomes.Indicate all relative distances that can be estimated.Note that NF1 is one of the genes you can map inthis way.c. Another mechanism that can lead to neurofibromasin this patient is a mitotic error producing cells with45 rather than the normal 46 chromosomes. Howcan this mechanism cause tumors? How do youknow, just from the results described, that none ofthese 20 tumors is formed by such mitotic errors?d. Can you think of any other type of error that couldproduce the results described?
. Neurofibromas are tumors of the skin that can arise
when a skin cell that is originally NF1+/ NF1− loses
the NF1+ allele. This wild-type allele encodes a functional protein (called a tumor suppressor), while the
NF1− allele encodes a nonfunctional protein.
A patient of genotype NF1+ / NF1− has 20 independent tumors in different areas of the skin. Samples
are taken of normal, noncancerous cells from this
patient, as well as of cells from each of the 20 tumors.
Extracts of these samples are analyzed by a technique
called gel electrophoresis that can detect variant
forms of four different proteins (A, B, C, and D) all
encoded by genes that lie on the same autosome as
NF1. Each protein has a slow (S) and a fast (F) form
that are encoded by different alleles (for example, AS
and AF
). In the extract of normal tissue, slow and fast
variants of all four proteins are found. In the extracts
of the tumors, 12 had only the fast variants of proteins
A and D but both the fast and slow variants of proteins B and C; 6 had only the fast variant of protein A
but both the fast and slow variants of proteins B, C,
and D; and the remaining 2 tumor extracts had only
the fast variant of protein A, only the slow variant of
protein B, the fast and slow variants of protein C, and
only the fast variant of protein D.
a. What kind of genetic event described in this chapter could cause all 20 tumors, assuming that all the
tumors are produced by the same mechanism?
b. Draw a genetic map describing these data, assuming that this small sample represents all the types
of tumors that could be formed by the same mechanism in this patient. Show which alleles of which
genes lie on the two homologous chromosomes.
Indicate all relative distances that can be estimated.
Note that NF1 is one of the genes you can map in
this way.
c. Another mechanism that can lead to neurofibromas
in this patient is a mitotic error producing cells with
45 rather than the normal 46 chromosomes. How
can this mechanism cause tumors? How do you
know, just from the results described, that none of
these 20 tumors is formed by such mitotic errors?
d. Can you think of any other type of error that could
produce the results described?
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