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. 2015 Jan 28;101(4):860–869. doi: 10.3945/ajcn.114.097279

TABLE 2.

Frequency of NTDs as a function of embryonic Shmt1 genotype1

Embryo Shmt1+/+
Embryo Shmt1+/−
Embryo Shmt1−/−
Diet and maternal genotype NTDs, n (%) Embryos, n NTDs, n (%) Embryos, n NTDs, n (%) Embryos, n
C 0 (0) 31 0 (0) 62 0 (0) 27
 Shmt1+/+ 0 (0) 31 0 (0) 36
 Shmt1−/− 0 (0) 26 0 (0) 27
C+T 0 (0) 25 0 (0) 63 0 (0) 32
 Shmt1+/+ 0 (0) 25 0 (0) 35
 Shmt1−/− 0 (0) 28 0 (0) 32
C+U 1 (2.9) 35 6 (10.3) 58 1 (3.9) 26
 Shmt1+/+ 1 (2.9) 35 4 (11.8) 34
 Shmt1−/− 2 (8.3) 24 1 (3.9) 26
C+dU 0 (0) 16 0 (0) 50 0 (0) 27
 Shmt1+/+ 0 (0) 16 0 (0) 23
 Shmt1−/− 0 (0) 27 0 (0) 27
FD 0 (0) 22 6 (12.2) 49 2 (9.5) 21
 Shmt1+/+ 0 (0) 22 1 (5.0) 20
 Shmt1−/− 5 (17.2) 29 2 (9.5) 21
FD+T 1 (4.6) 22 2 (4.4) 45 2 (14.3) 14
 Shmt1+/+ 1 (4.6) 22 1 (3.7) 27
 Shmt1−/− 1 (5.6) 18 2 (14.3) 14
FD+U 2 (8.0) 25 5 (8.9) 56 6 (30.0) 20
 Shmt1+/+ 2 (8.0) 25 2 (6.5) 31
 Shmt1−/− 3 (12.0) 25 6 (30.0) 20
FD+dU 0 (0) 17 0 (0) 50 0 (0) 18
 Shmt1+/+ 0 (0) 17 0 (0) 21
 Shmt1−/− 0 (0) 29 0 (0) 18
1

Frequency of NTDs observed in litters isolated from crosses of Shmt1-deficient mice on a 129/SvEv background on gestational day 11.5. The effect of embryo genotype on NTD occurrence was not significant (P > 0.05). A set of a priori hypotheses between diets (C+T, C+U, and C+dU vs. C; FD vs. C; FD+T, FD+U, and FD+dU vs. FD) within each embryo genotype was tested by using exact tests. A Bonferroni correction was applied as a correction for multiple comparisons. C, control diet; C+dU, control diet supplemented with 2′-deoxyuridine; C+T, control diet supplemented with thymidine; C+U, control diet supplemented with uridine; FD, AIN-93G lacking folic acid; FD+dU, folate-deficient diet supplemented with 2′-deoxyuridine; FD+T, folate-deficient diet supplemented with thymidine; FD+U, folate-deficient diet supplemented with uridine; NTD, neural tube defect; —, embryonic genotype not observed from these dams.