AI Article Synopsis
- Four mutant clones from the Y1 mouse adrenocortical tumor cell line show adenylyl cyclase (AC) activity that does not respond to forskolin, a direct AC activator.
- Analysis revealed that all four mutants lack AC-4, while other AC isoforms (AC-1, AC-3, and AC-5/6) remain at normal levels compared to the original Y1 cells.
- Introducing AC-4 into one of the mutant clones restored forskolin's effects on cAMP signaling, cell morphology, and growth, highlighting AC-4's crucial role in forskolin responsiveness in this cell line.
Article Abstract
Four mutant clones independently derived from the Y1 mouse adrenocortical tumor cell line have adenylyl cyclase (AC) activities that are resistant to forskolin, a direct activator of AC. In this study the AC isoform composition of the forskolin-resistant mutants was examined in order to explore the underlying basis for the resistance to forskolin. As determined by Western blot and RT-PCR analysis, the four forskolin-resistant mutants all were deficient in AC-4; the levels of other AC isoforms (AC-1, AC-3 and AC-5/6) were comparable to the levels in parent Y1 cells. Transfection of one of the mutant clones with an AC-4 expression vector increased forskolin-stimulated cAMP signaling, and restored forskolin-induced changes in cell morphology and growth. Taken together, these observations indicate that AC-4 deficiency is a hallmark of the forskolin-resistant phenotype of these mutants and suggest that AC-4 is an important target of forskolin action in the Y1 adrenal cell line.
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| http://dx.doi.org/10.1016/j.mce.2003.10.066 | DOI Listing |
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