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Pathogen research abs 1 || Pathogen research abs 2 || Pathogen research abs 3 || Pathogen research abs 4 || Pathogen research abs 5 || Hormone and endocrine research abs 1 || Hormone and endocrine research abs 2 || Hormone and endocrine research abs 3 || Hormone and endocrine research abs 4 || Hormone and endocrine research abs 5

Gen Comp Endocrinol. 2003 Jun 15;132(2):333-47.
Cloning of cDNAs encoding the three pituitary glycoprotein hormone beta subunit precursor molecules in the Japanese toad, Bufo japonicus.

Komoike Y, Ishii S.

Department of Biology, School of Education, Waseda University, 1-6-1 Nishi-waseda, Shinjuku, Tokyo 169-8050, Japan. komoikuou.waseda.jp

Complementary DNAs encoding precursor molecules of the beta subunits of three pituitary glycoprotein hormones (LH, FSH, and TSH) of the Japanese toad (Bufo japonicus) were isolated and sequenced. Unexpectedly large numbers of single nucleotide substitutions were found in all three beta subunit cDNAs. The eight isolated LH beta precursor cDNA clones were classified into six forms of nucleotide sequence, with four nucleotide substitutions each in the apoprotein coding region and in the 3' untranslated region (UTR). In the deduced amino acid sequence, the LH beta subunit showed two forms with a single amino acid substitution. The seven isolated FSH beta subunit cDNAs were classified into two forms, which differed from each other at 11 positions in the 3' UTR. The six isolated TSH beta subunit clones were classified into four forms with 2 and 5 nucleotide substitutions in the signal peptide and apoprotein coding regions, respectively. However, all the substitutions in the apoprotein coding region were silent. The substitution in the signal peptide coding region could produce three forms of signal peptide. Amino acid sequence comparison revealed that the toad LH beta subunit is more similar to the fish GTH II beta subunit than to mammalian and avian LH beta subunits. We found that the toad LH beta subunit molecule is a partial chimera of LH and FSH; amino acid residues located in 36th to 42nd and 96th to 99th are identical or similar to those of not LH- but FSH-beta subunit in mammalian, whereas it is more similar to LH- than FSH-beta subunit in total. We also found that the toad FSH beta subunit is more similar to the fish GTH II beta subunit than to the fish GTH I beta subunit and that the toad TSH beta subunit is more similar to tetrapod TSH beta subunits than to fish TSH beta subunits.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12812782&dopt=Abstract [PubMed - in process]

Dev Biol. 2003 Jul 1;259(1):1-8.
Coordinate regulation of small temporal RNAs at the onset of Drosophila metamorphosis.

Bashirullah A, Pasquinelli AE, Kiger AA, Perrimon N, Ruvkun G, Thummel CS.

Howard Hughes Medical Institute, Department of Human Genetics, 15 North 2030 East Room 5100, University of Utah, Salt Lake City, UT 84112-5331, USA.

The lin-4 and let-7 small temporal RNAs play a central role in controlling the timing of Caenorhabditis elegans cell fate decisions. let-7 has been conserved through evolution, and its expression correlates with adult development in bilateral animals, including Drosophila [Nature 408 (2000), 86]. The best match for lin-4 in Drosophila, miR-125, is also expressed during pupal and adult stages of Drosophila development [Curr. Biol. 12 (2002), 735]. Here, we ask whether the steroid hormone ecdysone induces let-7 or miR-125 expression at the onset of metamorphosis, attempting to link a known temporal regulator in Drosophila with the heterochronic pathway defined in C. elegans. We find that let-7 and miR-125 are coordinately expressed in late larvae and prepupae, in synchrony with the high titer ecdysone pulses that initiate metamorphosis. Unexpectedly, however, their expression is neither dependent on the EcR ecdysone receptor nor inducible by ecdysone in cultured larval organs. Although let-7 and miR-125 can be induced by ecdysone in Kc tissue culture cells, their expression is significantly delayed relative to that seen in the animal. let-7 and miR-125 are encoded adjacent to one another in the genome, and their induction correlates with the transient appearance of an approximately 500-nt RNA transcribed from this region, providing a mechanism to explain their precise coordinate regulation. We conclude that a common precursor RNA containing both let-7 and miR-125 is induced independently of ecdysone in Drosophila, raising the possibility of a temporal signal that is distinct from the well-characterized ecdysone-EcR pathway.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12812783&dopt=Abstract

Dev Biol. 2003 Jul 1;259(1):9-18.
Temporal regulation of microRNA expression in Drosophila melanogaster mediated by hormonal signals and broad-Complex gene activity.

Sempere LF, Sokol NS, Dubrovsky EB, Berger EM, Ambros V.

Department of Genetics, Dartmouth Medical School, Hanover, NH 03755, USA.

lin-4 and let-7 are founding members of an extensive family of genes that produce small transcripts, termed microRNAs (miRNAs). In Caenorhabditis elegans, lin-4 and let-7 control the timing of postembryonic events by translational repression of target genes, permitting progression from early to late developmental programs. To identify Drosophila melanogaster miRNAs that could play similar roles in the control of developmental timing, we characterized the developmental expression profile of 24 miRNAs in Drosophila, and found 7 miRNAs that are either upregulated or downregulated in conjunction with metamorphosis. The upregulation of three of these miRNAs (mir-100, mir-125, and let-7), and the downregulation of a fourth (mir-34) requires the hormone ecdysone (Ecd) and the activity of the Ecd-inducible gene Broad-Complex. Interestingly, mir-125 is a putative homologue of lin-4. mir-100, -125, and let-7 are clustered within an 800-bp region on chromosome 2L, suggesting that these three miRNAs may be coordinately regulated via common cis-acting elements during metamorphosis. In S2 cells, Ecd and the juvenile hormone analog methoprene exert opposite effects on the expression of these four miRNAs, indicating the participation of both these hormones in the temporal regulation of mir-34, -100, -125, and let-7 expression in vivo.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12812784&dopt=Abstract

Dev Biol. 2003 Jul 1;259(1):19-33.
Sox10 regulates the development of neural crest-derived melanocytes in Xenopus.

Aoki Y, Saint-Germain N, Gyda M, Magner-Fink E, Lee YH, Credidio C, Saint-Jeannet JP.

Department of Animal Biology, School of Veterinary Medicine, University of Pennsylvania, 3800 Spruce Street, Philadelphia, PA 19104, USA.

The transcription factors of the Sox family play important roles in diverse developmental processes. A number of genetic studies have established that Sox10 is a major regulator of neural crest formation. Here, we report the cloning and functional analysis of the Xenopus Sox10 gene. Sox10 mRNA accumulates during gastrulation at the lateral edges of the neural plate, in the neural crest-forming region. In this tissue, Sox10 expression is regulated by Wnt signaling and colocalizes with two major regulators of neural crest formation, Slug and Sox9. While initially expressed in neural crest cells from all axial levels, at the tailbud stage, Sox10 is downregulated in the cranial neural crest and persists mostly in neural crest cells from the trunk region. Overexpression of Sox10 causes a dramatic expansion of the Slug expression domain. We show that the C-terminal portion of Sox10 is sufficient to mediate this activity. Later during embryogenesis, Sox10-injected embryos show a massive increase in pigment cells (Trp-2-expressing cells). The responsiveness of the embryo to Sox10 overexpression by expansion of the Slug expression domain and ectopic production of Trp-2-positive cells and differentiated melanocytes is lost during gastrulation, as revealed by a hormone-inducible Sox10 construct. These results suggest that Sox10 is involved in the specification of neural crest progenitors fated to form the pigment cell lineage.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12812785&dopt=Abstract

Dev Biol. 2003 Jul 1;259(1):71-82.
Nifedipine reveals the existence of two discrete components of the progesterone-induced [Ca2+]i transient in human spermatozoa.

Kirkman-Brown JC, Barratt CL, Publicover SJ.

School of Biosciences, The University of Birmingham, Birmingham B15 2TT, UK. j.kirkmanbrowham.ac.uk

The steroid progesterone, an agonist of acrosome reaction, induces a biphasic [Ca(2+)](i)-signal in human sperm comprising an initial transient [Ca(2+)](i) elevation, and a subsequent ramp or plateau. Nifedipine, an inhibitor of voltage-operated Ca(2+) channels, inhibits progesterone-induced acrosome reaction in human sperm, but fluorimetric studies have detected no effect of this compound on the progesterone-induced [Ca(2+)](i) signal. We have used single-cell imaging to study the effects of nifedipine on [Ca(2+)](i) signalling in human sperm. Analysis of mean responses from large numbers of cells showed that treatment with nifedipine reduced the duration but not the amplitude of the progesterone-induced [Ca(2+)](i) transient. In control cells, the latency of the transient peak (maximum fluorescence) fell within the range of 30-105 s. In the presence of nifedipine, very few cells peaked "late" (>60 s after application of progesterone). Analysis of transient responses in control cells revealed characteristic "early" and "late" responses, most cells showing both "early" and "late" transients, whereas "late" transients were rare and smaller in the presence of nifedipine. Sustained responses showed strong association with late transients, and occurrence and amplitude of sustained responses were significantly reduced in nifedipine pretreated cells.These findings are consistent with the occurrence of a discrete, nifedipine-sensitive component of the progesterone-induced [Ca(2+)](i) transient that peaks 1-2 min after exposure to the hormone and is crucial for the induction of the sustained [Ca(2+)](i) signal.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12812789&dopt=Abstract

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