Correct option is B
The incorrect statement is (b). CaM Kinase II does not require continuous calcium (Ca²⁺) and calmodulin to remain active. While it is initially activated by Ca²⁺ and calmodulin, CaM Kinase II has the ability to become autophosphorylated, which allows it to stay active even after the calcium signal has disappeared. This ability to remain active without the continuous presence of calcium is an essential feature of its role in memory and synaptic plasticity. Therefore, CaM Kinase II does not require calcium and calmodulin to remain active once it has been autophosphorylated.
Information Booster:
- Autophosphorylation of CaM Kinase II allows it to maintain its active state even after the initial calcium signal has ceased. This feature is critical for the molecular memory function of CaM Kinase II, as it enables the kinase to "remember" past calcium oscillations and to continue its signaling without needing the presence of calcium or calmodulin. This is a key mechanism for synaptic plasticity and the persistence of long-term changes in neuronal activity.
- The autophosphorylation makes CaM Kinase II an ideal molecular memory device because it allows the enzyme to integrate the frequency and duration of calcium pulses and encode this information in its continued activity. This property is important for learning and memory processes like long-term potentiation (LTP).
Additional Information:
- CaM Kinase II activity increases as a function of Ca²⁺ pulse frequency: This statement is correct. The activity of CaM Kinase II does indeed increase with higher frequencies of calcium pulses. The kinase acts as a frequency decoder, where the frequency of calcium oscillations influences its activation and subsequent cellular responses.
- A brain-specific CaM Kinase II knockout mouse will have difficulty in remembering where things are: This is correct. Mice lacking CaM Kinase II specifically in the brain show impairments in memory, particularly spatial memory, as CaM Kinase II is involved in synaptic plasticity and encoding information for memory storage.
- The molecular memory function is lost in an autophosphorylation defective CaM Kinase II: This is also correct. Autophosphorylation is a key mechanism that allows CaM Kinase II to function as a molecular memory device. Without this function, the kinase cannot remain active after the calcium signal ceases, and its role in synaptic plasticity and memory is impaired.
