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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Gene Review: 

Pard6a  -  par-6 family cell polarity regulator alpha

Mus musculus

Synonyms: 0710008C04Rik, 2610010A15Rik, PAR-6, PAR-6 alpha, PAR-6A, ...
 
 
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High impact information on Pard6a

  • Nuclear movement was unaffected by the inhibition of dynein, Par6, or PKCzeta, yet these components were essential for MTOC reorientation, as they maintained the MTOC at the cell centroid [1].
  • Furthermore, pVHL interacts with the Par3-Par6-atypical PKC complex, suggesting a mechanism for linking polarity pathways to microtubule capture and ciliogenesis [2].
  • PKCzetaII is shown to interact with the Par6 protein and functions in the development of cell polarity [3].
  • This behavior is also controlled by Cdc42 via the Par6/protein kinase Czeta pathway [4].
  • We detected asymmetric distribution of Par6 protein in relation to the site of meiosis, but not sperm entry [5].
 

Anatomical context of Pard6a

  • These results suggest that Cdc42 and Par6 negatively regulate TJ assembly in mammalian epithelial cells [6].
  • Assembly of epithelial tight junctions is negatively regulated by Par6 [6].
  • Here, we show that Par6 inhibits TJ assembly in MDCK II epithelial cells after their disruption by Ca(2+) depletion but does not inhibit adherens junction (AJ) formation [6].
  • Interestingly, PAR-6, aPKC, CRB3 and Pals1, but not PAR-3 or PATJ, were also concentrated on the apical membranes in differentiated cells [7].
  • Here we show that two PAR6-related proteins have distinct polarized distributions in mouse oocytes. mPARD6a is first localized on the spindle and then accumulates at the pole nearest the cortex during spindle migration [8].
 

Physical interactions of Pard6a

  • However, the absence of PALS1 and PATJ expression did result in the decreased association of CRB3 with members of the Par6/Par3/aPKC protein complex [9].
 

Other interactions of Pard6a

  • The Par proteins (partitioning-defective) Par3 and Par6, plus atypical protein kinase C (aPKC) function in the formation or maintenance of TJs and more generally in metazoan cell polarity establishment [6].
  • The atypical PKCs (aPKCs) have been implicated genetically in at least two independent signaling cascades that control NF-kappa B and cell polarity, through the interaction with the adapters p62 and Par-6, respectively [10].

References

  1. Nuclear movement regulated by Cdc42, MRCK, myosin, and actin flow establishes MTOC polarization in migrating cells. Gomes, E.R., Jani, S., Gundersen, G.G. Cell (2005) [Pubmed]
  2. The von Hippel-Lindau tumor suppressor protein controls ciliogenesis by orienting microtubule growth. Schermer, B., Ghenoiu, C., Bartram, M., M??ller, R.U., Kotsis, F., H??hne, M., K??hn, W., Rapka, M., Nitschke, R., Zentgraf, H., Fliegauf, M., Omran, H., Walz, G., Benzing, T. J. Cell Biol. (2006) [Pubmed]
  3. Identification of PKCzetaII: an endogenous inhibitor of cell polarity. Parkinson, S.J., Le Good, J.A., Whelan, R.D., Whitehead, P., Parker, P.J. EMBO J. (2004) [Pubmed]
  4. Cdc42 mediates nucleus movement and MTOC polarization in Swiss 3T3 fibroblasts under mechanical shear stress. Lee, J.S., Chang, M.I., Tseng, Y., Wirtz, D. Mol. Biol. Cell (2005) [Pubmed]
  5. First cleavage of the mouse embryo responds to change in egg shape at fertilization. Gray, D., Plusa, B., Piotrowska, K., Na, J., Tom, B., Glover, D.M., Zernicka-Goetz, M. Curr. Biol. (2004) [Pubmed]
  6. Assembly of epithelial tight junctions is negatively regulated by Par6. Gao, L., Joberty, G., Macara, I.G. Curr. Biol. (2002) [Pubmed]
  7. Behavior of tight-junction, adherens-junction and cell polarity proteins during HNF-4alpha-induced epithelial polarization. Satohisa, S., Chiba, H., Osanai, M., Ohno, S., Kojima, T., Saito, T., Sawada, N. Exp. Cell Res. (2005) [Pubmed]
  8. Two PAR6 proteins become asymmetrically localized during establishment of polarity in mouse oocytes. Vinot, S., Le, T., Maro, B., Louvet-Vallée, S. Curr. Biol. (2004) [Pubmed]
  9. Loss of PALS1 expression leads to tight junction and polarity defects. Straight, S.W., Shin, K., Fogg, V.C., Fan, S., Liu, C.J., Roh, M., Margolis, B. Mol. Biol. Cell (2004) [Pubmed]
  10. The atypical PKC-interacting protein p62 is an important mediator of RANK-activated osteoclastogenesis. Durán, A., Serrano, M., Leitges, M., Flores, J.M., Picard, S., Brown, J.P., Moscat, J., Diaz-Meco, M.T. Dev. Cell (2004) [Pubmed]
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