Signal transduction protein P(II) is dephosphorylated in Synechocystis sp. strain PCC 6803 by protein phosphatase PphA.
First-pass extracted concept
P(II)
Aliases
nonphosphorylated P(II), signal transduction protein P(II)
Evidence Snippets
Supporting Sources
Linked Claims
The P(II)-dependent control mechanism can be bypassed by exposing cells to excess nitrate.
This control mechanism can be bypassed by exposing cells to excess levels of nitrate.
In Synechocystis sp. strain PCC 6803, PphA dephosphorylates P(II).
Signal transduction protein P(II) is dephosphorylated in Synechocystis sp. strain PCC 6803 by protein phosphatase PphA.
Mutants lacking either PphA or P(II) are impaired in efficient utilization of nitrate as the nitrogen source.
Mutants lacking either PphA or P(II) were impaired in efficient utilization of nitrate as the nitrogen source.
Uncontrolled nitrate uptake causes light-dependent nitrite excretion even in wild-type cells, supporting that nitrate uptake controls nitrate utilization under limiting photon flux densities.
Uncontrolled nitrate uptake leads to light-dependent nitrite excretion even in wild-type cells, confirming that nitrate uptake controls nitrate utilization in response to limiting photon flux densities.
Under limiting PSI-reduced ferredoxin, P(II) signaling mutants show excess nitrate reduction, impaired nitrite reduction, and nitrite excretion to the medium.
Under conditions of limiting photosystem I (PSI)-reduced ferredoxin, excess reduction of nitrate along with impaired reduction of nitrite occurred in P(II) signaling mutants, resulting in excretion of nitrite to the medium.
Nonphosphorylated P(II) controls nitrate utilization in response to low light intensity by tuning down nitrate uptake to match actual reduction capacity.
We present evidence that nonphosphorylated P(II) controls the utilization of nitrate in response to low light intensity by tuning down nitrate uptake to meet the actual reduction capacity.
Increasing the level of PSI-reduced ferredoxin reverses the nitrite-excretion-related effect observed in P(II) signaling mutants.
This effect could be reversed by increasing the level of PSI-reduced ferredoxin.