Table 1 Continued Fold change . 3 7 . 3 7 . 3 6 . 3 4 . 3 3 . 3 2 Gene symbol Fah Mpzl2 Insl3 Wif1 Inha Gene title Fumarylacetoacetate hydrolase Myelin protein zero-like 2 Insulin-like 3 Wnt inhibitory factor 1 Inhibin a Col18a1 Procollagen, type XVIII, a 1 Transcripts up-regulated 72 h after start of treatment 35.0 Drd4 Dopamine receptor 4 21.1 Slc38a5 Solute carrier family 38a5 14.9 Rhox5 Reproductive homeobox 5 13.9 Fabp5 Fatty acid binding protein 5, epidermal 8.4 Spinlw1 Eppin 7.6 Klk1b24 Kallikrein 1-related peptidase b24 6.6 Tubb3 Tubulin, b 3 5.9 Hdc Histidine decarboxylase 5.5 Fah Fumarylacetoacetate hydrolase 5.5 Tsx Testis speciﬁc X-linked gene 5.4 Zcchc18 Zinc ﬁnger, CCHC domain 18 4.6 Sct Secretin 4.6 Gpd1 Glycerol-3-phosphate dehydrogenase 1 4.5 Myh1 Myosin, heavy polypeptide 1 4.5 Fabp4 Fatty acid binding protein 4, adipocyte 4.5 St8sia2 ST8 sialyltransferase 2 4.5 Tgfb1 Transforming growth factor, b 1 4.3 Pscdbp Pleckstrin homology binding protein 4.2 Igf1 Insulin-like growth factor 1 . 4 1 . 4 1 . 4 0 . 4 0 . 4 0 . 3 9 . 3 8 . 3 8 . 3 8 . 3 7 . 3 7 Scara5 Sept6 D17H6- S56E-5 Pappa Klk1 Dmkn Tpd52l1 Inha Slc25a5 Car3 Pde4b Scavenger receptor class A, member 5 Septin 6 Chr 17, human D6S56E 5 Pregnancy-associated plasma protein A Kallikrein 1 Dermokine Tumour protein D52-like 1 Inhibin a Solute carrier family 25, member 5 Carbonic anhydrase 3 Phosphodiesterase 4B, cAMP speciﬁc Effects of FSH on testicular transcript levels . M H ABEL and others 295 Fold Gene change symbol Gene title . 4 9 . 4 9 . 4 9 . 4 8 . 4 7 . 4 7 . 3 6 . 3 6 . 3 6 . 3 5 . 3 5 . 3 4 . 3 4 . 3 3 Hsd17b11 Hydroxysteroid (17b) dehydrogenase 11 Cabc1 Chaperone, ABC1 complex-like 9630031F1- RIKEN cDNA 9630031F12 gene 2Rik Ptch1 Patched homolog 1 Smoc2 SPARC related modular calcium binding 2 Fhod3 Formin homology 2 domain containing 3 Transcripts down-regulated 72 h after start of treatment 13.4 Igfbp3 Insulin-like growth factor binding protein 3 8.2 Rgs11 Regulator of G-protein signalling 11 6.6 Rin2 Ras and Rab interactor 2 6.5 Clca1 Chloride channel calcium activated 1 6.0 Slc40a1 Solute carrier family 40 1 5.6 Spsb1 splA receptor domain and SOCS box 1 4.9 Iﬁtm1 Interferon induced transmembrane 1 4.7 Myh8 Myosin, heavy polypeptide 8 4.6 Fhod3 Formin homology 2 domain containing 3 4.4 Bcan Brevican 4.4 Tmem140 Transmembrane protein 140 4.4 BC013672 cDNA sequence BC013672 4.3 Tmem37 Transmembrane protein 37 4.0 Erbb3 v-erb-b2 homolog 3 3.9 Dst Dystonin 3.9 Xist Inactive X speciﬁc transcripts 3.8 Arhgdig Rho GDP dissociation inhibitor g 3.7 Edn1 Endothelin 1 3.7 6330403- RIKEN cDNA 6330403K07 gene K07Rik 3.7 Jun Jun oncogene 3.6 Pla2g5 Phospholipase A2, group V 3.6 Apbb2 Amyloid b precursor protein-binding B2 H19 Hspb1 Fcgr2b Adi1 H2-T23 Scin Rnasel H19 fetal liver mRNA Heat shock protein 1 Fc receptor, IgG, low afﬁnity IIb Transcribed locusc Acireductone dioxygenase 1 Histocompatibility 2, T region locus 23 Scinderin Ribonuclease L aIf a transcript is represented more than once on the array only the highest fold change is shown in this table. Supplementary Table 2 shows the complete signiﬁcant dataset. bNet affy number 1454967_at. cNet affy number 1436092_at. Kingma et al. 1998, Perera et al. 2001, Dettin et al. 2003, Jiang et al. 2006) and, perhaps surprisingly, in the Leydig cells (e.g. Ren1, Cyp17a1, Akr1b7, Star, Ldlr and Nr4a1; Deschepper et al. 1986, Le Goascogne et al. 1991, Song et al. 2001, Baron et al. 2003; Table 1). By 24 h after the start of FSH treatment, androgen-dependent Sertoli cell transcripts appeared in the list of up-regu- lated transcripts (e.g. Rhox5, Drd4, Spinlw1 and Tubb3; Lindsey & Wilkinson 1996, Cunningham et al. 1998, Denolet et al. 2006, O’Shaughnessy et al. 2007) and this www.endocrinology-journals.org trend became more marked by 72 h. By contrast with the somatic cells, very few germ cell genes appear on the lists of signiﬁcantly regulated transcripts. Only Hdc (increased 4.0- and 5.9-fold at 24 and 72 h respectively; Saﬁna et al. 2002) and 1700021K02Rik (Spatial ) (increased 3.1-fold at 72 h) (Irla et al. 2003) were signiﬁcantly altered by FSH within the time-span of these studies (Table 1 and Supplementary Table 2). Few of the transcripts down-regulated following FSH treatment have been localised in the testis with the Journal of Molecular Endocrinology (2009) 42, 291–303