In mammals, the dark color of skin, hair, and eyes is due to a pigment called melanin. Melanin is produced by specialized skin cells called melanocytes. The melanin is then transferred to other skin cells called keratinocytes. Melanocytes synthesize melanin in a multistep metabolic pathway (Figure 1). The amount of melanin produced is dependent on the amount of the enzymes TYR, TRP2, and TRP1 present inside melanocytes.
Figure 1. Melanin
synthesis pathway
The peptide hormone α-melanocyte stimulating hormone (α-MSH) activates a signal transduction pathway leading to the activation of MITF. MITF is a transcription factor that increases the expression of the TYR, TRP2, and TRP1 genes (Figure 2).
Some mammals increase melanin production in response to ultraviolet (UV) radiation. The UV radiation causes damage to DNA in keratinocytes, which activates the p53 protein. p53 increases the expression of the POMC gene. The POMC protein is then cleaved to produce α-MSH. The keratinocytes secrete α-MSH, which signals nearby melanocytes. The increased melanin absorbs UV radiation, reducing further DNA damage.
Which of the following claims about the TYR, TRP2, and TRP1 mammalian genes is most likely to be accurate?
In mammals, the dark color of skin, hair, and eyes is due to a pigment called melanin. Melanin is produced by specialized skin cells called melanocytes. The melanin
is then transferred to other skin cells called keratinocytes. Melanocytes synthesize melanin in a multistep metabolic pathway (Figure 1). The amount of melanin produced is dependent on the amount of the enzymes TYR, TRP2, and TRP1 present inside melanocytes.
Figure 1. Melanin synthesis pathway
The peptide hormone α-melanocyte stimulating hormone (α-MSH) activates a signal transduction pathway leading to the activation of MITF. MITF is a transcription factor that increases the expression of
the TYR, TRP2, and TRP1 genes (Figure 2).
In mammals, the dark color of skin, hair, and eyes is due to a pigment called melanin. Melanin is produced by specialized skin cells called melanocytes. The melanin is then transferred to other skin cells called keratinocytes. Melanocytes synthesize melanin in a multistep metabolic pathway (Figure 1). The amount of melanin produced is dependent on the amount of the enzymes TYR, TRP2, and TRP1 present inside melanocytes.
Figure 1. Melanin synthesis
pathway
The peptide hormone α-melanocyte stimulating hormone (α-MSH) activates a signal transduction pathway leading to the activation of MITF. MITF is a transcription factor that increases the expression of the TYR, TRP2, and TRP1 genes (Figure 2).
Which of the following claims best explains why keratinocytes do not produce melanin?
In mammals, the dark color of skin, hair, and eyes is due to a pigment called melanin. Melanin is produced by
specialized skin cells called melanocytes. The melanin is then transferred to other skin cells called keratinocytes. Melanocytes synthesize melanin in a multistep metabolic pathway (Figure 1). The amount of melanin produced is dependent on the amount of the enzymes TYR, TRP2, and TRP1 present inside melanocytes.
Figure 1. Melanin synthesis pathway
The peptide hormone α-melanocyte stimulating hormone (α-MSH) activates a signal transduction pathway leading to the activation of MITF. MITF is
a transcription factor that increases the expression of the TYR, TRP2, and TRP1 genes (Figure 2).
Figure 2. Activation of melanin synthesis genes in melanocytes
Some mammals increase melanin production in response to ultraviolet (UV) radiation. The UV radiation causes damage to DNA in keratinocytes, which activates the p53 protein. p53 increases the expression of the POMC gene. The POMC protein is then cleaved to produce α-MSH. The keratinocytes secrete α-MSH, which signals nearby
melanocytes. The increased melanin absorbs UV radiation, reducing further DNA damage.
Mice have melanocytes in the skin on their ears and show a tanning response to UV radiation. Researchers were studying a mutant population of mice that do not show a tanning response. Genetic testing of these mutant mice showed that the pathway causing the production of α-MSH by keratinocytes in response to UV radiation was fully functional. Thus, the researchers claimed that the lack of tanning response was due a nonfunctional MC1R.
Which of the following pieces of evidence would best support the researchers' claim above?
In mammals, the dark color of skin, hair, and eyes is due to a pigment called melanin. Melanin is produced by specialized skin cells called melanocytes. The melanin is then transferred to other skin cells called keratinocytes. Melanocytes synthesize melanin in a multistep metabolic pathway (Figure 1). The amount of melanin
produced is dependent on the amount of the enzymes TYR, TRP2, and TRP1 present inside melanocytes.
Figure 1. Melanin synthesis pathway
The peptide hormone α-melanocyte stimulating hormone (α-MSH) activates a signal transduction pathway leading to the activation of MITF. MITF is a transcription factor that increases the expression of the TYR, TRP2, and TRP1 genes (Figure 2).
Some mammals increase melanin production in response to ultraviolet (UV) radiation. The UV radiation causes damage to DNA in keratinocytes, which activates the p53 protein. p53 increases the expression of the POMC gene. The POMC protein is then cleaved to produce α-MSH. The keratinocytes secrete α-MSH, which signals nearby melanocytes. The increased melanin absorbs UV radiation, reducing further DNA damage.
Based on the information provided in Figure 1 and Figure 2, which of the following best predicts the effects of a mutation in the promoter of the TYR gene that prevents it from being transcribed?
In mammals, the dark color of skin, hair, and eyes is due to a pigment called melanin. Melanin is produced by specialized skin cells called melanocytes. The melanin is then transferred to other skin cells called keratinocytes. Melanocytes synthesize melanin in a multistep metabolic pathway (Figure 1). The amount of melanin produced is dependent on the amount of the enzymes TYR, TRP2, and TRP1 present inside melanocytes.
Figure 1. Melanin synthesis
pathway
The peptide hormone α-melanocyte stimulating hormone (α-MSH) activates a signal transduction pathway leading to the activation of MITF. MITF is a transcription factor that increases the expression of the TYR, TRP2, and TRP1 genes (Figure 2).
Some mammals increase melanin production in response to ultraviolet (UV) radiation. The UV radiation causes damage to DNA in keratinocytes, which activates the p53 protein. p53 increases the expression of the POMC gene. The POMC protein is then cleaved to produce α-MSH. The keratinocytes secrete α-MSH, which signals nearby melanocytes. The increased melanin absorbs UV radiation, reducing further DNA damage.
Which of the following best explains a process occurring between point 1 and point 2 in Figure 3 ?
In mammals, the dark color of skin, hair, and eyes is due to a pigment called melanin. Melanin is produced by specialized skin cells called melanocytes. The melanin is then transferred to
other skin cells called keratinocytes. Melanocytes synthesize melanin in a multistep metabolic pathway (Figure 1). The amount of melanin produced is dependent on the amount of the enzymes TYR, TRP2, and TRP1 present inside melanocytes.
Figure 1. Melanin synthesis pathway
The peptide hormone α-melanocyte stimulating hormone (α-MSH) activates a signal transduction pathway leading to the activation of MITF. MITF is a transcription factor that increases the expression of the TYR, TRP2, and
TRP1 genes (Figure 2).
Some mammals increase melanin production in response to ultraviolet (UV) radiation. The UV radiation causes damage to DNA in keratinocytes, which activates the p53 protein. p53 increases the expression of the POMC gene. The POMC protein is then cleaved to produce α-MSH. The keratinocytes secrete α-MSH, which signals nearby melanocytes. The increased melanin absorbs UV radiation, reducing further DNA damage.
Researchers discovered a mutant form of the TYR gene with
a deletion of a single guanine nucleotide in the beginning of the coding sequence.
Which of the following best predicts the phenotype of an individual who is homozygous for this TYR mutation?