Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.7.11.22 (cdc2)
 8,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Progression of BY-2 tobacco cells through the cell cycle was followed after treatments with ultra violet (UV) and salicylic acid (SA) used as a potent inhibitor of the octadecanoid pathway which can mediate response to UV irradiation. Cells in S phase were more sensitive than G0/G1 or G2 cells to UV irradiation. Although SA efficiently blocked cells in G0/G1 or G2, it did not block S phase synchronized cells. UV and SA applied simultaneously to cells in G0/G1 delayed the cell cycle progression more than each one separately. Therefore UV irradiation and SA act as agonists to arrest BY-2 cells at cell cycle entry. To further investigate the signalling pathway mediating UV response, we complemented a UV-sensitive Escherichia coli strain with a Nicotiana xanthi cDNA expression library. A cDNA (arcA3) whose coding sequence is identical to the 2,4-D induced arcA cDNA cloned by Ishida et al. (1993) was isolated. We show that arcA3 transcription is induced at cell cycle entry but not directly by the 2,4-D treatment. Moreover, arcA3 transcription is induced prior to the restriction point as shown with the CDK inhibitor roscovitine. The arcA3 transcription level is increased by UV irradiation but prevented by SA. Indeed, addition of SA prior to UV irradiation blocks the induction of arcA3 transcription. This suggests that arcA3 gene is modulated in both UV and SA responses, the SA effect preceding the UV step. Since arcA3 is 67% similar to RACK1 (functional homology), a rat intracellular receptor for protein kinase C, and possesses identical PKC fixation motifs, it is hypothesised that the arcA3 gene is involved in UV and SA cell cycle arrest.
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PMID:Is arcA3 a possible mediator in the signal transduction pathway during agonist cell cycle arrest by salicylic acid and UV irradiation? 1008 53

P34(cdc2) is a key cell-cycle protein in fission yeast that is necessary for progress in the cell cycle from the G1 to the S phase and from G2 through mitosis. Homologues of p34(cdc2) have been found in all eukaryotes that have been investigated. Levels of p34(cdc2)-like protein were studied by quantitative Western blotting in developing cotyledons of Daucus carota L. (carrot) seedlings, in expiants from the same seedlings transferred to tissueculture media with and without 2,4-dichlorophenoxyacetic acid (2,4-D), and in nutrient-starved suspension cultures derived from carrot callus. During the cessation of cell division, which accompanies development of the cotyledon to maturity, there was a 16-fold decline in the level of the p34(cdc2)-like protein. Auxin-stimulated dedifferentiation in excised tissue from mature cotyledons was accompanied by restoration of the level of p34(cdc2)-like protein, and the responding cells formed a callus. These data support our earlier proposition, based upon evidence from wheat leaf, that changes in the level of p34(cdc2)-like protein act in the switch between cycling and differentiation. Persisting high levels of p34(cdc2)-like protein in suspension cultures, when division was stopped by nutrient limitation, indicated that decline of the protein was not an inevitable consequence of the cessation of division. Decline of p34(cdc2) in differentiation may therefore be a regulated process that determines exit from the cell cycle and the converse increase in p34(cdc2) may be a regulated process controlling dedifferentiation and resumption of cell division.
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PMID:Levels of p34(cdc2)-like protein in dividing, differentiating and dedifferentiating cells of carrot. 2418 10