Table I.

Summary of the effect of different gain and loss-of-function constructs on LGN and NuMA distribution, spindle orientation, and production of ectopic neural progenitors

ConditionLGN distributionbNuMA distributionSpindle orientationEctopic progenitors at E4c
Wild typeLateral cortical ringCortical ring/spindle polesPlanar
LGN RNAiNo ring/spindle polesRandom++a
Ct-LGNCytoplasmicaNo ring/spindle polesRandoma++a
LGN RNAi + mLGN rescueNDNDPlanar (wild type)aa
NuMA RNAiCorticalDefects+
Gαi1/2 RNAiNDNDDefects+
PTx-ANDNDDefects++
ratGαi1-G203AStrong corticalNo ring/faint cortical?/spindle polesRandom++
ratGαi1Strong corticalNDND++
Cyto-ratGαi1NDNDND++
ratGαi2NDNDND++
ratGαi3NDNDND++
Human GαtransducinNDNDND++
ratGαolfNDNDND
ratGαolf-G213ACortical (wild type)NDPlanar (wild type)
  • ND, not determined.

  • a Morin et al, 2007.

  • b Data from overexpression of GFP-tagged chick LGN or Myc-tagged mouse LGN.

  • c Ectopic progenitors are determined by the presence of BrdU+ cells in the mantle zone on transverse sections at E4 after a 45-min BrdU pulse (see Morin et al, 2007).