Table 2

Maternal Par4 deficiency rescues Thbd−/− embryos from growth arrest at E8.5

Breeding pairsEmbryonic genotypeThbd+/+Thbd+/−Thbd−/−
Par4−/−Thbd+/− female × Thbd+/− male; n = 50, analysis at 9.5 dpc Par4+/− 10 29 11 
Par4−/−Thbd+/− female × Thbd+/− male; n = 64, term pups Par4+/− 25 33 
Par4−/−Thbd+/− × Par4−/−Thbd+/−; n = 51, analysis at 9.5 dpc Par4−/− 40 
Breeding pairsEmbryonic genotypeThbd+/+Thbd+/−Thbd−/−
Par4−/−Thbd+/− female × Thbd+/− male; n = 50, analysis at 9.5 dpc Par4+/− 10 29 11 
Par4−/−Thbd+/− female × Thbd+/− male; n = 64, term pups Par4+/− 25 33 
Par4−/−Thbd+/− × Par4−/−Thbd+/−; n = 51, analysis at 9.5 dpc Par4−/− 40 

Pregnancies were analyzed at 9.5 dpc or at term, as indicated. Numbers represent embryos that had progressed beyond Theiler stage 13 by the time of analysis (9.5 dpc) or normal-appearing term pups (in term analyses). Absence of maternal Par4 resulted in Thbd−/− embryos that had progressed beyond Theiler stage 13, but several of these were smaller in size and only half of them presented with beating hearts at the time of dissection (Figure S1). Normal Thbd−/− neonates were born at about one-third of expected Mendelian frequency. Simultaneous absence of maternal and fetal Par4 did not improve the yield of rescued E9.5 Thbd−/− embryos.

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