Table 1

Foxl2-null ("KO") ovaries relative to wild-type and in various biological contexts.

A. Down in Foxl2 KO (induced by Foxl2)


rank

Single Foxl2 KO

Compound Foxl2 KOs

Single Foxl2 KO and compound Foxl2 KO

Foxl2 single KO and Wnt4 single KO


1

(Foxl2)

(Foxl2)

(Foxl2)

(Foxl2)

2

    Thbs2

Nupr1

    Ntn4

Thbs2

3

Peg10

    Thbs1

    Thbs1

Kitl

4

    Sdc4

Ephx2

    Adamts16

Gstm1

5

    Fbn2

1810010m01rik/ZG-16p

Col8a1

Cpa2

6

9630031f12rik

Loc640441

Clstn2*

Il13ra2

7

Akr1c14

Cyp19a1/aromatase

Cpa2

ENSMUSG00000069372

8

    Ntn4

Dppa3

    Smad3

Peg10

9

Cdkn1b

Myo1b

    Slc26a7

Tnfrsf19

10

    Thbs1

    Ramp1

Chst9

9630031F12Rik

11

E330037m01rik

    Slc26a7

Loc640441

Micalcl

12

Col8a1

Col8a1

Lrrc4*

Dync1i1

13

    Adamts16

Plxnc1*

Bcat1

Fbn2

14

Serpine2

    Ntn4

Itga6

Gpc4

15

Clstn2*

Clstn2*

Il13ra2

Gstm7

16

Grip1

Odz4*

Nupr1

Fbn2

17

Speer4b

Apoa1

Plxnc1*

Upk2

18

Rgs2

Bcat1

    Angptl6

Cdkn1b

19

Cpa2

Lrrc4*

    Chn2

Akr1c14

20

Lmo3

Pdpn

Odz4*

Tmem20

B. Up in Foxl2 KO (repressed by, or competitive with Foxl2)

rank

Single Foxl2 KO

Compound Foxl2 KOs

Single Foxl2 KO and compound Foxl2 KO

Foxl2 single KO and Wnt4 single KO

1

Jakmip1

Tesc

Adamts8

Inhbb

2

Slc8a3

Pnmt

Hsd17b11

Fbln2

3

B3galt6

Dmrt1

Fbln2

Dhh

4

Rps9

Sox9

Dhh

Ndrg2

5

2010004m13rik

Gm2a

2310046k01rik

Ptn

6

Hemgn

BC021891

Nr0b1/Dax1

Tpm2

7

Ndrg1

Etv5

4632411j06rik

Stra6

8

Mmp23

Mmd2

Ifitm7

Thbd

9

Ptpre

Fxyd6

Gas7

Myl1

10

Tnni3

Etv5

Mcm7

Scn5a

11

Inhbb

Cyp26b1

Efhd1

Col6a2

12

Efhd2

Il6st

Il6st

LOC669875///Tspan15

13

Ermap

Ecrg4

Dsp

Adi1

14

Adamts8

Itm2a

Bc019731

Adamts8

15

Lgals1

Fbln2

Gm2a

Tpm2

16

Dmpk

Dhh

1500015o10rik/Ecrg4

Aqp5

17

Hsd17b11

Bc019731

Mmd2

Gtl2

18

Eraf

D3bwg0562e

Cdon

Dsp

19

Wnt11

Gpc3

2810026p18rik

Gna14

20

Slc4a1

40787

Dusp26

Filip1


The twenty top-ranking genes showing significant down- or up-regulation (upper, A, vs lower half, B, of the table, resp.) in Foxl2-null ("KO") ovaries relative to wild-type and in various biological contexts. From left to right, top-ranking genes are given for the following conditions: ovaries lacking only Foxl2 (aged 13.5 dpc to birth); shared between newborn ovaries lacking Foxl2 and Kit and those lacking Foxl2 and Wnt4; shared by all three models (that all involve Foxl2 loss); and shared between embryo-fetal ovaries lacking Foxl2 and those lacking Wnt4 alone [Foxl2 ranks at the top because one or more of the conditions under analysis involve its ablation]. Genes known to be expressed in vasculature or germ cells are underlined, neuronal genes have an asterisk, and testis (lower, B) and other genes of interest (upper, A) are in bold font.

Garcia-Ortiz et al. BMC Developmental Biology 2009 9:36   doi:10.1186/1471-213X-9-36

Open Data