The blue light receptor Phototropin 1 suppresses lateral root growth by controlling cell elongation.

We investigated the relationship between the blue light receptor phototropin 1 (phot1) and lateral root growth in Arabidopsis thaliana seedlings. Fluorescence and confocal microscopy images, as well as PHOT1 mRNA expression studies provide evidence that it is highly expressed in the elongation zone of lateral roots where auxin is accumulating. However, treatment with the auxin transport inhibitor N-1-naphthylphthalamic acid significantly reduced PHOT1 expression in this zone. In addition, PHOT1 expression was higher in darkness than in light. The total number of lateral roots was higher in the phot1 mutant than in wild-type Arabidopsis. Cells in the elongation zone of lateral roots of the phot1 mutant were longer than those of wild-type lateral roots. These findings suggest that PHOT1 plays a role(s) in elongation of lateral roots through the control of an auxin-related signalling pathway.

Allergenicity of recombinant profilins from Japanese hop, Humulus japonicus.

BACKGROUND AND OBJECTIVE: Pollen from Japanese hop, Humulusjaponicus, is a major cause of pollinosis in Korea. Profilin (15 kDa) from Humulus scandens has been associated with strong allergenicity in allergic Chinese patients. Profilin has also been detected in pollen extract from Korean Japanese hop by proteomic analysis and immunoglobulin (Ig) E immunoblotting. However, the allergenicity of allergens isolated from Japanese hop has not been investigated in Korean individuals. This study was undertaken to produce recombinant profilin from Japanese hop and evaluate its allergenicity. METHODS: Complementary DNA sequences encoding 2 isoallergens were cloned by reverse transcription polymerase chain reaction and their recombinant proteins expressed in Escherichia coli. The IgE-binding reactivities of the recombinant allergens were assessed by enzyme-linked immunosorbent assay. RESULTS: The deduced amino acid sequences of the H. japonicus profilins were 68.7% to 80.2% homologous with profilins from mugwort (Art v 4), ragweed (Amb a 14), and birch (Bet v 2). Two isoallergens of profilin from H. japonicus were 78.2% identical. Notably, the cDNA sequences of these 2 isoallergens were 98.5% (AY268422) and 98.7% (AY268424) identical to those of H. scandens. Serum samples from Japanese hop-sensitized individuals showed 12.9% IgE reactivity to both of the recombinant profilin isoallergens from H. japonicus, indicating that profilin may not be an allergenically dominant component of Japanese hop pollen. The recombinant profilins showed only 0% to 9.3% inhibition of the crude extract. CONCLUSIONS: Two isoallergens of profilin that are highly conserved with those of mugwort, ragweed, and birch were identified in H. japonicus. Profilins from Japanese hop pollen may play a minor role in the pathogenesis of pollinosis in Koreans.

l-Ascorbic acid 2-phosphate promotes elongation of hair shafts via the secretion of insulin-like growth factor-1 from dermal papilla cells through phosphatidylinositol 3-kinase.

BACKGROUND: l-Ascorbic acid 2-phosphate (Asc 2-P), a derivative of l-ascorbic acid, promotes elongation of hair shafts in cultured human hair follicles and induces hair growth in mice. OBJECTIVES: To investigate whether the promotion of hair growth by Asc 2-P is mediated by insulin-like growth factor-1 (IGF-1) and, if so, to investigate the mechanism of the Asc 2-P-induced IGF-1 expression. METHODS: Dermal papilla (DP) cells were cultured and IGF-1 level was measured by reverse transcription-polymerase chain reaction and enzyme-linked immunosorbent assay after Asc 2-P treatment in the absence or presence of LY294002, a phosphatidylinositol 3-kinase (PI3K) inhibitor. Also, hair shaft elongation in cultured human scalp hair follicles and proliferation of cocultured keratinocytes were examined after Asc 2-P treatment in the absence or presence of neutralizing antibody against IGF-1. In addition, keratinocyte proliferation in cultured hair follicles after Asc 2-P treatment in the absence or presence of LY294002 was examined by Ki-67 immunostaining. RESULTS: IGF-1 mRNA in DP cells was upregulated and IGF-1 protein in the conditioned medium of DP cells was significantly increased after treatment with Asc 2-P. Immunohistochemical staining showed that IGF-1 staining is increased in the DP of cultured human hair follicles by Asc 2-P. The neutralizing antibody against IGF-1 significantly suppressed the Asc 2-P-mediated elongation of hair shafts in hair follicle organ culture and significantly attenuated Asc 2-P-induced growth of cocultured keratinocytes. LY294002 significantly attenuated Asc 2-P-inducible IGF-1 expression and proliferation of follicular keratinocytes in cultured hair follicles. CONCLUSIONS: These data show that Asc 2-P-inducible IGF-1 from DP cells promotes proliferation of follicular keratinocytes and stimulates hair follicle growth in vitro via PI3K.

Cloning and characterization of GITR ligand.

The gene encoding the natural ligand of murine glucocorticoid-induced tumor necrosis factor receptor (GITR) was cloned and characterized. The putative GITR ligand (GITRL) is composed of 173 amino acids with features resembling those of type II membrane proteins and is 51% identical to the human activation-inducible TNF receptor (AITR) ligand, TL6. Expression of the GITRL is restricted to immature and mature splenic dendritic cells. GITRL binds GITR expressed on HEK 293 cells and triggers NF-kappaB activation. Functional studies reveal that soluble CD8-GITRL prevents CD4+CD25+ regulatory T-cell-mediated suppressive activities.

Inhibition effect of new farnesol derivatives on all-trans-retinoic acid metabolism.

All-trans-retinoic acid (atRA) is a promising anticancer and antiwrinkle drug. However, its clinical application is limited because it is rapidly metabolized by the induced cytochrome P450 (P450). In this study, farnesol derivatives are proposed as new inhibitors to prevent P450-mediated metabolism. The farnesol derivatives were suc-farnesol and mal-farnesol, which were synthesized by the chemical conjugation of farnesol with succinic anhydride and maleic anhydride, respectively. The inhibition effects of farnesol, farnesoic acid, and farnesol derivatives on the atRA metabolism were evaluated in microsome and in AMC-HN-6 cells. In the microsome experiment, suc-farnesol and mal-farnesol strongly inhibited atRA metabolism at 10(minus;4) mol/L concentration by as much as 61% and 77%, respectively. In the cell experiment, the inhibition effects of farnesol derivatives on the atRA metabolism showed similar tendency as the results in the microsome experiment, even if the effect was somewhat decreased. Effects of farnesoic acid and farnesol, however, were not significant. This research suggests that carboxylic end groups, such as atRA and hydrophobicity, might be important factors causing the higher inhibition effect, and that derivatization of farnesol can be 1 method to develop new inhibitors of atRA metabolism.

The roles of two TATA boxes and 3'-flanking region of soybean beta-tubulin gene (tubB1) in light-sensitive expression.

The soybean tubB1 gene is expressed primarily in the germinating seedling and is strongly down regulated in response to light in the upper hypocotyl. Previous studies demonstrate that the 1 kb 5'-flanking region of this gene is sufficient for its appropriate expression in etiolated seedlings. Transient expression studies demonstrated that the presence of the tubB1 3'-flanking sequence element decreased reporter gene expression as compared to the nopaline synthase (NOS) 3'-flanking sequence element. In this study we investigated the ability of the 3' flanking region to influence the expression of a beta-glucuronidase (GUS) reporter gene in transgenic tobacco and Arabidopsis. The presence of the tubB1 3'-flanking sequence element in chimera constructs reduced reporter gene expression specifically in the hypocotyl and petioles of light-grown, transgenic seedlings. Additionally, site-directed mutagenesis of the two TATA sequences in the 1 kb tubB1 5'-flanking sequence element (TATA box A in the -122 to -117 bp region and TATA box B in the -35 to -30 region) showed that both elements are functional and additive in controlling tubB1 gene expression in seedling tissues. While transcription from TATA box A was predominant regardless of lighting conditions, the relative usage of TATA box B increased in the dark. We conclude that both TATA box sequences are utilized to direct expression of the tubB1 gene to the cotyledons, hypocotyl and root tip of germinating seedlings that are regions of cell expansion and that the 3'-flanking sequence element down-regulates expression in the hypocotyl in response to light. Thus, it is plausible that the tubB1 protein may play an important role in cell expansion in seedling development requiring its regulated expression by light.

Capsaicin protects against ethanol-induced oxidative injury in the gastric mucosa of rats.

In this study, we investigated the protective effects of capsaicin on gastric mucosal oxidative damage induced by ethanol. Sprague Dawley rats intragastrically received 0.5-10 mg/kg, BW capsaicin or vehicle; 30 min later gastric lesions were induced by intragastric administration of absolute ethanol. Lipid peroxidation was estimated by measuring thiobarbituric acid reactive substances in gastric mucosa. Myeloperoxidase activity, a marker enzyme of polymorphonuclear leukocytes for tissue inflammation, was also measured in the gastric mucosa. The expression level of cyclooxygenase-2, which increases in inflammatory region, was determined by Western blot analysis. Capsaicin significantly suppressed gastric haemorrhagic erosions induced by ethanol. Capsaicin inhibited lipid peroxidation and myeloperoxidase activity in ethanol-induced gastric mucosal lesion in a dose-dependent manner. Capsaicin also inhibited the expression of cyclooxygenase-2 in the gastric mucosal lesion. The gastroprotective activity of capsaicin on the ethanol-induced oxidative damage may be important for chemoprevention.

Low molecular weight protamine: a potent but nontoxic antagonist to heparin/low molecular weight protamine.

To avoid bleeding complications, protamine is routinely used after cardiovascular surgery to neutralize the anticoagulant function of heparin. However, its clinical use is associated with adverse and sometimes fatal reactions. Based on literature review of the mechanism of heparin neutralization and protamine induced immunologic toxicity, we propose the following hypothesis: If a chain shortened low molecular weight protamine (LMWP) containing the heparin neutralizing domain could be derived from native protamine, it could be a potent and yet nontoxic heparin antagonist. In this study, we present results to validate this hypothesis. LMWP fragments containing an intact arginine sequence and an average molecular weight of approximately 1,100 daltons were successfully prepared by enzymatic digestion of protamine with thermolysin. In vitro studies show that such LMWP fragments completely neutralized the anticoagulant functions of heparin and LMWH, based on the anti-Xa chromogenic and aPTT clotting time assays. In vivo results reveal that although injection of protamine to mice led to obvious production of anti-protamine antibodies, injection of LMWP did not elicit any detectable immunogenic responses. In addition, these LMWP fragments exhibited a markedly reduced antigenicity and cross-reactivity toward the mice anti-protamine antibodies.

Effects of capsaicin on induction of c-jun proto-oncogene expression in Fisher-344 rats by N-methyl-N'-nitro-N-nitrosoguanidine.

N-Methyl-N'-nitro-N-nitrosoguanidine (MNNG) is a potent inducer of cellular stress leading to chromosomal aberrations, point mutations, and cell death. To study the effect of capsaicin on c-jun expression when given with MNNG to rats, Fisher-344 rats that had been administered MNNG were treated with capsaicin in their diet and organs were removed for measuring c-jun transcripts. We show that pre- or post-treatment of capsaicin relative to MNNG administration up- or down-regulates (depending on the organ) c-jun expression in a consistent pattern in most organs. In fact, we found in this study that capsaicin inhibits c-jun induction, stimulated by MNNG, in the spleen, heart, stomach and lung. Since MNNG, a methylating agent, is a powerful carcinogen that is very effective in the induction of c-jun mRNA, the results suggest that capsaicin uptake in the diet could play a role in inhibition of tumorigenesis induced by MNNG.

The induction of P450-mediated oxidation of all-trans retinoic acid by retinoids in head and neck squamous cell carcinoma cell lines.

All-trans retinoic acid (RA) can be catabolized into polar metabolites by cytochrome P450 (P450) in several tissues including the skin. We examined eight different squamous cell carcinoma (SCC) cell lines to determine their capacity to induce P450-mediated oxidation of RA. Among the eight different cell lines, enhanced catabolism was detected in AMC-HN-1, -2, -5, and -6, whereas it was not found in the cell lines of AMC-HN-3, -4, -7, and -8. It was found that the enhanced catabolism brought on by P450 induction was blocked when RA was added to AMC-HN-6 along with actinomycin D or cyclohexamide. Also, this catabolism was inhibited by ketoconazole. P450-mediated oxidation was detectable within 4 hours of RA treatment, and RA catabolism reached its maximum 16 hours after treatment. P450 was induced by 13-cis-RA, 9-cis-RA, and retinal; however, retinol could not induce P450. In conclusion, P450 can be induced by retinoids in head and neck SCC (HNSCC) cells and the ability of retinoids to induce P450 can serve as an important factor in determining the biological effect of retinoids.

Brain-derived neurotrophic factor rapidly potentiates synaptic transmission through NMDA, but suppresses it through non-NMDA receptors in rat hippocampal neuron.

Brain-derived neurotrophic factor (BDNF) rapidly enhances synaptic transmission among the hippocampal neurons. In order to examine which component of glutamate receptors participates in synaptic potentiation by BDNF, we have studied the effect of glutamate antagonists on excitatory postsynaptic currents (EPSCs) enhanced by BDNF, using cultured embryonic hippocampal neurons. In the presence of AP5, a N-methyl-D-aspartate (NMDA) antagonist, BDNF depressed the EPSCs. In contrast, BDNF enhanced the EPSCs in the presence of a non-NMDA antagonist CNQX. Our results suggest that BDNF acutely activates synaptic transmission via NMDA, but suppresses it via non-NMDA receptors in the hippocampus.

Arabidopsis NPH1: a protein kinase with a putative redox-sensing domain.

The NPH1 (nonphototropic hypocotyl 1) gene encodes an essential component acting very early in the signal-transduction chain for phototropism. Arabidopsis NPH1 contains a serine-threonine kinase domain and LOV1 and LOV2 repeats that share similarity (36 to 56 percent) with Halobacterium salinarium Bat, Azotobacter vinelandii NIFL, Neurospora crassa White Collar-1, Escherichia coli Aer, and the Eag family of potassium-channel proteins from Drosophila and mammals. Sequence similarity with a known (NIFL) and a suspected (Aer) flavoprotein suggests that NPH1 LOV1 and LOV2 may be flavin-binding domains that regulate kinase activity in response to blue light-induced redox changes.

Capsaicin can alter the expression of tumor forming-related genes which might be followed by induction of apoptosis of a Korean stomach cancer cell line, SNU-1.

Capsaicin (CAP) has been known to inhibit some tumor development in vivo (J.J. Jang, S.H. Kim, T.K. Yun, Inhibitory effect of capsaicin on mouse lung tumor development, in vivo, J. Korean Med. Sci. 3 (1989) 49-53; J.J. Jang, K.J. Cho, Y.S. Lee, J.H. Bae, Different modifying responses of capsaicin in a wide-spectrum initiation model of F344 rat, J. Korean Med. 6 (1991) 31-36) [1,2] even though its mechanism of action is not well understood. The objectives of this study were to examine the effect of CAP on expression of tumor forming-related genes in a Korean stomach tumor cell, SNU-1. We used slot blot hybridization to investigate its effect on a wide spectrum of proto-oncogenes. It was found that CAP enhanced the transcripts of two proto-oncogenes (c-myc and c-Ha-ras) and tumor suppressor gene p53. While a low concentration of CAP (0.01 microM) did not significantly increase the level of p53 transcript in SNU-1, it did increase it by a factor of 3.5 at a 10 microM dose of CAP. Consequently, SNU-1 cells are sensitive to CAP in the overexpression of tumor suppressor gene, p53 and proto-oncogenes, c-myc and c-Ha-ras, but not those of c-erbB-2, c-jun and bcl-2 genes. Both cell death and DNA fragmentation were shown in SNU-1 cells with treatment of CAP. Our results suggest that CAP induces apoptotic cell death in human gastric cancer cells (SNU-1) in vitro which may be possibly mediated by the overexpression of p53 and/or c-myc genes. Because cell suicide is arguably the most potent natural defense against cancer, the correlation between the induction of apoptosis and the change of tumor forming-related gene expression after CAP treatment should be further studied in detail.

Selective monitoring of peptidase activities with synthetic polypeptide substrates and polyion-sensitive membrane electrode detection.

A novel method to monitor specific peptidase activities in biological samples as complex as undiluted plasma/blood is described. The approach is based on the design of synthetic polypeptide substrates in which di- or triarginine sequences are linked to each other via one or more other amino acids recognized specifically by the peptidase to be determined. Detection of chymotrypsin and renin activities using synthetic substrates P4 (F-R-R-R-F-V-R-R-F-NH2) and P5 (R-R-R-L-L-R-R-L-L-R-R-R), respectively, serves to demonstrate the principles of this new assay system. A polyion-sensitive membrane electrode, prepared by doping polymer films with dinonylnaphthalene-sulfonate (DNNS), is shown to exhibit significant nonequilibrium electromotive force (EMF) responses toward these and other polycationic substrates at microgram/milliliter levels under physiological conditions. The same electrode, however, exhibits much smaller total EMF response toward the shorter fragments of the synthetic peptides generated by peptidase activity; hence, the addition of peptidase to a solution containing the synthetic substrate yields a change in electrode EMF response, the rate of which is proportional to the activity of peptidase present. Other synthetic polycationic peptides as well as natural polycationic peptides (e.g., protamine) that lack specific cleavage sites for chymotrypsin and renin, yet are detected by the DNNS-based membrane electrode, do not elicit any significant change in EMF response in the presence of the peptidases, confirming the feasibility and utility of the proposed bioanalytical method.

Highly specific cytochrome P450-like enzymes for all-trans-retinoic acid in T47D human breast cancer cells.

When human breast cancer T47D cells were treated with all-trans-retinoic acid (RA), the RA 4- and 18-hydroxylase activities were induced in microsomes in a time-dependent manner, indicating that these cells readily metabolized RA into more polar compounds, such as all-trans-4-hydroxy-RA and all-trans-18-hydroxy-RA. In contrast, T47D cells treated for 12 h with xenobiotics, such as phenobarbital, beta-naphthoflavone, 3-methylcholanthrene, and dimethylsulfoxide, showed lower levels of catalytic activities for 4- and 18-hydroxylases. The induction of 4- and 18-hydroxylase activities appears to be regulated at the level of transcriptional control (basal level). Competitive assays demonstrated that inhibitors and substrates for 1A, 2A, 3A, 2B, and 2C cytochrome P450 (P450 subfamilies), all-trans-retinol, and all-trans-retinal showed no inhibition of RA metabolism, but other retinoic acid derivatives competed highly with RA. The RA-inducible 4- and 18-hydroxylases showed high specificity for RA and high levels of catalytic activities, with Km and maximum velocity values for 4-hydroxylase equal to 99 nmol/L and 0.26 pmol/min.mg protein, respectively, and those for 18-hydroxylase equal to 65 nmol/L and 0.18 pmol/min.mg protein. Cell-free metabolism of RA required microsomes from RA-treated cells and NADPH, and was inhibited by liarozole, an inhibitor of P450. These data suggest that RA-inducible 4- and 18-hydroxylases may be novel P450 isozymes.

Homogeneous enzyme-based binding assay for studying glycosaminoglycan interactions with macromolecules and peptides.

A simple and rapid homogeneous enzyme-based binding assay is described to study the degree of interaction between glycosaminoglycans and various macromolecules/peptides. The method is based on the homogeneous inhibition of a highly positively charged enzyme, acid deoxyribonuclease II (EC 3.1.22.1), by glycosaminoglycan polyanions, such as heparin, chondroitin 4-sulfate, and dermatan sulfate. Catalytic activity of DNase II is inhibited to nearly 100% by relatively small amounts of these glycosaminoglycan molecules. In the presence of species that bind these polyanions, the activity of the enzyme is regained in an amount proportional to the concentration of the species present. Thus, the relative binding affinities of various species with a given GAG can be assessed rapidly by comparing the concentration of the compound required to reverse the enzyme inhibition to 50% of the maximum value (ED(50) values). The feasibility of this binding assay principle is demonstrated by measuring the ED(50) values of five macromolecules: polylysine, polyarginine, protamine, low-density lipoprotein (LDL), and high-density lipoprotein (HDL), using heparins of different size, as well as chondroitin 4-sulfate and dermatan sulfate as the GAG polyanions. The applicability of the assay method is further extended to study GAG-peptide interactions. A variety of small synthetic peptides (8-13 amino acid residues) derived from the heparin-binding domains of protamine and type IV collagen are used as model peptide species. Relative GAG-binding affinities of these macromolecules/peptides are compared to previous literature values and data obtained via a new electrode-based titration method.

A protamine filter for extracorporeal heparin removal. Development, testing, blood compatibility evaluation, and future direction.

The authors previously developed a filter device containing immobilized protamine (termed "protamine filter") that could be used to remove heparin during extracorporeal perfusion. In vivo studies involving dogs showed that the protamine filter removed more than 50% of heparin from the animals' blood circuit in less than 20 min. In addition, the use of the protamine filter did not elicit statistically significant protamine induced hemodynamic and thrombocytopenic responses. Biocompatibility of the protamine filter was also evaluated, with the focus on its effect on the coagulation cascade, the complement system, and the blood antithrombin III levels. Results showed that heparin adsorbed to the protamine coated surface retained 20% of its original activated partial thromboplastin time activity, rendering the coated surface antithrombotic. Activation of the coagulation system by the protamine coated membrane and the untreated cellulose membrane, as measured by the elevation of prothrombin fragment F1 + 2 levels, was statistically identical. The CH50 hemolytic assay showed that the protamine coated membrane produced a reduction of 1.2 +/- 0.8% of the total complement levels, as compared to 9.4 +/- 1.6% by the untreated membrane. In addition, the change in C3a des Arginine levels after 30 min of circulation was 1.5 +/- 0.2 mg/ml by the protamine filter, as compared to 2.1 +/- 0.1 mg/ml by the untreated membrane. Unlike native heparin that would bind with antithrombin, heparin adsorbed on the protamine coated surface was devoid of such activity, and produced no depletion of circulating antithrombin. Because of the limited capacity of the protamine filter, the future system is envisioned to consist of two filters; while one filter is removing heparin the other will be regenerated. With a recently developed heparin sensor, it should be possible to design a sensor directed, biofeedback, two filter heparin removal system.

Hypocotyl expression and light downregulation of the soybean tubulin gene, tubB1.

The tubB1 beta-tubulin gene of Glycine max (previously named s beta 1) is highly expressed only in rapidly elongating regions of etiolated seedling hypocotyls and this expression is strongly downregulated when the seedlings are exposed to light. Primer extension demonstrated that the gene was transcribed in these tissues and contained two sites of transcriptional initiation. To determine the mechanism regulating tubB1 expression, a chimeric reporter gene was constructed by fusing 5' upstream regions of tubB1 to a promoterless beta-glucuronidase (GUS) gene and these constructs were introduced into protoplasts by electroporation. Strong transient expression of the reporter gene was obtained after electroporation of chimeric constructs containing 1 kb of tubB1 5' upstream sequence into tobacco protoplasts. Deletion of the distal most 300 bp from the 5' sequence of tubB1 enhanced expression, suggesting the possibility of a negative transcriptional regulator in this region. Additional deletions of the 5' sequence reduced expression substantially. Constructs containing a tubB1 3' terminus were expressed at much lower levels than those containing a nopaline synthase (NOS) 3' terminus. The tubB1-GUS chimeric gene also was introduced into tobacco by Agrobacterium-mediated Ti plasmid transformation and the organ-specific expression pattern of the chimeric gene was determined in seedlings of the transgenic plants. Hypocotyls exhibited strong GUS activity when the seedlings were germinated in darkness, but lacked the GUS enzyme when the seedlings were germinated in the light.(ABSTRACT TRUNCATED AT 250 WORDS)

Basic fibroblast growth factor is a testicular germ cell product which may regulate Sertoli cell function.

Previously, a proteinacious factor secreted by a mixture of rat testicular spermatocytes and round spermatids was shown to stimulate transferrin mRNA and protein levels in Sertoli cells. To identify the germ cell-secreted proteins which affect Sertoli cell functions, concentrated germ cell-conditioned medium was fractionated by reverse-phase HPLC. The fraction which eluted at 35% acetonitrile increased transferrin secretion in Sertoli cell cultures 2.4-fold above the basal level. Both the active fraction and a protein extract from cultured germ cells were positive for basic fibroblast growth factor (bFGF) as determined by Western blot analysis and immunoprecipitation. The apparent molecular sizes of the immunoreactive proteins were 30, 27, and 24 kilodaltons (kDa). By immunohistochemistry, bFGF was shown to be present in pachytene spermatocytes and Leydig cells. The bFGF receptor was also examined by immunohistochemistry and found to be present in Leydig cells, round and elongated spermatids, and Sertoli cells. The presence of receptors was more pronounced in stages I-VIII. Western blot analysis confirmed that the receptors were expressed in isolated round spermatids, elongated spermatids, and Sertoli cells. Two major receptor species with apparent molecular sizes of 120 and 145 kDa were detected in the rat testis. Germ cells contained both of these receptors, but Sertoli cells possessed only the 120-kDa receptor. From these experiments, it is evident that bFGF is a germ cell product which may regulate Sertoli cell function. The expression of bFGF and its receptor may be an important component of germ cell-Sertoli cell and/or germ cell-germ cell communication during spermatogenesis.