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

From: A mouse chromosome 4 balancer ENU-mutagenesis screen isolates eleven lethal lines

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]