Figure 8.

TGFβII negatively regulates amacrine cell genesis. (a,b) X-gal staining of E18.5 GLAST::CreERT2+/-;R26R reporter+ transgenic without (a) and with (b) administration of tamoxifen at E16. Inset in (a) shows GLAST immunostaining of E15.5 retina. (c-j) Analysis of TGFβRII+/-;GLAST::CreERT2+/-;R26R+ (c,e,g) and TGFβRII-/-;GLAST::CreERT2+/-;R26R+ (d,f,h,i,j) retinae immunostained with anti-TGFβRII (c,d), Pax6 (e,f) and syntaxin (g-j). Arrowheads in (i) mark ectopic amacrine cell clusters. TGFβRII-/- retinae in panels (d-h) and (i,j) are from two different mutant embryos. (k,l) E18.5 > 8DIV retinal explants cultured with vehicle control (k) or TGFβRII-Fc (l) and labeled with anti-Pax6. (m) Percentage of Pax6+ amacrine cells/field in vehicle control (black bar; 2,148 Pax6+ in 10 fields) and TGFβRII-Fc treated (white bar; 4,966 Pax6+ in 15 fields) retinal explants. (n,o) E18.5→8DIV wild-type (n) or Zac1+m/- (o) retinal explants cultured with rTGFβII. Asterisk in (o) indicates ECL formation in Zac1+m/- retinae even in the presence of rTGFβII. (p) Percentage of amacrine cells in wild-type explants (black bar; vehicle control: 1,761 Pax6+/3,353 DAPI+; rTGFβII: 2,605 Pax6+/4,301 DAPI+ in INL+GCL) and Zac1+m/-+ECL explants (white bar; vehicle control: 2,232 Pax6+/3,328 DAPI+; rTGFβII: 3,243 Pax6+/5,282 DAPI+ in INL+GCL).

Ma et al. Neural Development 2007 2:11   doi:10.1186/1749-8104-2-11
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