Why does the introduction of a liver-specific "activator" protein into a skin cell not immediately cause the skin cell to start producing all liver-specific proteins?

Question

Why does the introduction of a liver-specific "activator" protein into a skin cell not immediately cause the skin cell to start producing all liver-specific proteins?

BlackTom AI · Accepted Answer

Question restatement: Why doesn't introducing a liver-specific activator protein into a skin cell immediately trigger production of all liver-specific proteins?
Option 1: Skin cells do not contain the genes for liver proteins. While skin cells may not actively express those genes, they typically do carry the genetic information (the DNA) for liver proteins in their genome. The issue is not missing genes, but regulation of expression, so this statement is not accurate.
Option 2: The TATA box in skin cells has a different sequence than in liver cells. The TATA box is a core promoter element that is generally conserved across many cell types; regulatory issues are not usually due to tissue-specific differences in the TATA box sequence itself. This option misrepresents promoter architecture as the primary barrier here.
Option 3: Liver genes likely require a combination of several activators, not just one, to form an active transcription initiation complex. This reflects a core concept in transcriptional regulation: gene expression often depends on multiple transcription factors assembling at enhancers and promoters to recruit RNA polymerase and initiate transcription. A single activator may be insufficient to create the full initiation complex or overcome chromatin barriers, explaining why one liver-specific activator alone does not drive all liver gene expression.
Option 4: The liver activator will immediately be degraded by skin cell proteasomes. While protein stability matters, there is no general rule that a liver-specific activator would be rapidly degraded in a skin cell; even if degradation could occur, the main conceptual barrier is the need for multiple regulatory inputs to activate a set of liver genes, not a universal proteasomal destruction. This option overstates proteolysis as the primary reason.
Overall, the most accurate explanation centers on the necessity for multiple activators to cooperate in forming an active transcription initiation complex, rather than relying on a single factor or promoter sequence differences. This aligns with our understanding of combinatorial control of gene expression and chromatin context in different cell types.

Bio 93 Section CDE 2025 Final- Section E

Why does the introduction of a liver-specific "activator" protein into a skin cell not immediately cause the skin cell to start producing all liver-specific proteins?

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