meiosis

  1. Fig 20-8
  2. 20-9
  3. 20-10
  4. 20-11
  5. 20-12
  6. Synaptonemal complex
  7. 20-13
  8. 15-56
  9. 17-41
  10. Cyclin cycle
  11. Regulators of meiosis
  12. Frog and starfish models of release from arrest
  13. MAPKinase
  14. 17-41
  15. 17-44
  16. 17-42

 

Cells lacking wee1 go into mitosis too soon, in yeast, so are very small. Cells lacking CDC25 can’t divide. In all cells, the wee1 is an inhibitor of Cdc2cyclinB (also called  Cdk1cyclinB) as is Myt1 kinase since both of them phosphorylate the kinase. The Cdc25 is the phosphatase that removes the inhibitory Ps.  It is controlled by Polo kinase Plk. In meiosis I, wee1 is absent so after MI complete, no S phase because Cdc2-cyclinB is activated rapidly which prevents that. A special branch of the MAPkinase family with cMos (found only in oocytes and eggs-a mutant vmos is an oncogene found in somatic cells after viral infection) can activate the Cdk1 to restart the cycle with no S, but it becomes arrested at metaphase due to MAPK and c-Mos activation of cytostatic factor. It can be removed by Calpain, which is activated by Ca++ release at fertilization

 Meiosis notes:

 

  1. Germinal vesicle breakdown (GVBD) shows cdc2-cyclinB activation
  2. Arrested in end of prophaseI: maturation inducing hormone progesterone in frogs, 1 methyladenine in starfish cause GVBD

 

  1. Second arrest G1 metaphII, released by ca release and breakdown cytostatic factor.

 

  1. Cyclin B in immature eggs, but little wee1 and cyclin A, accum end meiI, little MAPK and PoloK

 

  1. CDC activated by cyclin B in M1 and by both cycB and cyc A in MII. CDC25 and MAPK stay same throughout

 

  1. MAPK and PoloK are activated same time as cdccyclinB. All inactivated by fertilization.

 

  1. MAPK controls  meiosis after reactivated:
  2. MeiosisI-II transition without an S by bypassing the inhibitory tyr P by activating CDCcyclinB rightaway, and also delay of breakdown of cyclinBCDC2, G1 arrest

 

  1. CDC25 activated by MAPK