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. 2009 Mar 6;10:12. doi: 10.1186/1471-2156-10-12

Table 4.

Previously published knockout alleles in the chromosome 4 (117–281) balancer

Gene Published phenotype
Pre-implantation

Cdca8
Cdc20
Faf1
embryos present at E3.5 but fail to form fully expanded blastocyst [8]
embryos arrested at the two cell stage [39]
embryos arrested at the two cell stage [12]
Nasp at E3.5, blastocyts are smaller with fewer cells [13]

E5.5–E8.5

Foxd3 failure to gastrulate, finger-like extensions seen at distal tip [14]
Gjb3 lethality before somite formation [15,16]
Hdac1 embryonic lethality before turning of embryo, growth retarded after E7.5 [17,18]
Macf1 lethality before somite formation [19]
Ncdn resorption was evident prior to E6.5 [20]
Urod lethality before somite formation, no fetuses at E7.5–E9.5 [21]

E9.5–E12.5

Bmp8b smaller than expected, delayed, die by E9.25 [22]
Ppap2b abnormal gastrulation, dead by E10.5 [23,24]
Slc2a1 prenatal lethality E10–E14, reduced embryo size, overall developmental delay [25]
Stil lethality around E10.5, abnormal left-right axis patterning, growth retardation abnormal neural tube morphology and development [26]
Tal1 lethality at E8.5–E10.5, arrested development, cardiovascular defects, defects in
hematopoiesis, distended pericardial sacs, pale and necrotic [9]

E13.5–E18.5

Dhcr24 some die before birth, others smaller with less adipose tissue, decreased cholesterol levels, male and female infertility [27]
Gjb5 death at E11.5–E14.5, smaller with placental defects [28]
Marcksl1 neural tube [29]
Mtf1 embryos die around E14 due to liver degeneration [30]
Ssbp3 prenatal lethality, abnormal head development [31]
Tie1 death before E13.5, respiratory, cardiovascular, skin defects [32]
Ybx1 lethality E13.5-just after birth, reduced embryo size, craniofacial defects, abnormal neural tube closure [33]

Peri-natal

Jak1 neonates smaller with abnormal B and T cell development [34]
Khdrbs1 2/3 die at birth, and the survivors live well into adulthood [35]
Nfia lethality at P0, survivors have severe brain abnormalities [36]
Pou3f1 die within a few hours of birth due to respiratory defects [37]
Ror1 die just after birth with abnormal blood chemistry and respiratory system defects [38]
Slc6a9 die just after birth with severe motor and respiratory defects[40]

Post-natal

Dab1 lethality at 20–30 days, decreased leptin levels, nervous system defects including ataxia, abnormal brain morphology [10,11]
Dmbx1 lethality before P9, smaller, little or no milk in stomachs [7,41,42]