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. Author manuscript; available in PMC: 2009 Nov 1.
Published in final edited form as: Dev Biol. 2008 Aug 29;323(1):6–18. doi: 10.1016/j.ydbio.2008.08.019

Table 1.

Suppression of the Cv2−/− lethal phenotype by Tsg loss-of-function. Genotypes of neonates obtained from Cv2+/−;Tsg+/− intercrosses.

Genotype Number of Embryos Observed percentage (Expected Percentage) Number of embryos with Cv2 skeletal phenotype* (%)
Cv2+/+ ; Tsg+/+ 8 9 (6.25)
Cv2+/− ; Tsg+/+ 12 14 (12.5)
Cv2+/+ ; Tsg+/− 9 10.5 (12.5)
Cv2+/− ; Tsg+/− 23 27 (25)
Cv2+/+ ; Tsg−/− 4 5 (6.25)
Cv2+/− ; Tsg−/− 8 9 (12.5)
Cv2−/− ; Tsg+/+ ** 5 6 (6.25) 5 (100%)
Cv2−/− ; Tsg+/− 9 10.5 (12.5) 8 (90%)
Cv2−/− ; Tsg−/− 8 9 (6.25) 0 (0%)

Total 86
*

Cv2 skeletal phenotypes include lack of the 13th rib and deltoid tuberosity, skull phenotype, and absence of the tracheal rings. Because defective neural arches and shorter tails are also found in Tsg mutants, this phenotype was not taken into account in this table.

**

all died as neonates

most died as neonates

some of these animals were recovered alive at day 3 post-partum; since these Cv2−/−;Tsg−/− mutants displayed the Tsg−/− skeletal phenotype we conclude that Tsg is genetically epistatic over Cv2. The rescue of the Cv2−/− phenotype in Cv2−/−;Tsg−/− was found to be statistically significant using a chi-square test for independence (p<0.001).

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