Molecular characterization of gonadotropin-inhibitory hormone (GnIH) gene and effect of intramuscular injection of GnIH peptide on the reproductive axis in Catla catla
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Title |
Molecular characterization of gonadotropin-inhibitory hormone (GnIH) gene and effect of intramuscular injection of GnIH peptide on the reproductive axis in Catla catla
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Creator |
Kumar P, Wisdom KS, Bhat IA, Gireesh-Babu P, Nayak SK, Reang D, Nagpure NS. and Sharma R
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Subject |
GnIH peptide; Catla catla; gene expression; annual reproductive cycle
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Description |
Not Available
Gonadotropin-inhibitory hormone (GnIH) plays an important role in reproduction by inhibiting the expression of gonadotropins in birds and mammals, but in fishes, it is ambiguous. In this study, we cloned 606 bp long cDNA of GnIH from Catla catla brain (cGnIH). The encoded preproGnIH peptide generated three putative peptides (cGnIH-I, -II, -III) of different size. Phylogenetic analysis of GnIH showed clustering of different peptide sequence with its orthologs in separate clades. The real-time PCR analysis showed the expression of cGnIH in brain, gonads, intestine, stomach, heart, gill and liver with the highest expression in the brain and gonads of both sexes. The basal GnIH mRNA expression was higher in spawning and spent phase of the male brain and spawning phase of the female brain. In testis, the expression was highest in spent phase, while in ovary the expression did not change significantly during reproductive phases. The in vivo experiment of cGnIH-III peptide exhibited the higher expression of HPG axis genes, lhb, fshb, cgnrh, kiss2 and kiss1r and serum hormonelevel of LH and FSH as soon as 3 h after the intramuscular delivery. These results suggest that the GnIH is positively involved in regulation of reproduction in HPG axis of C. catla Not Available |
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Date |
2022-06-15T10:59:07Z
2022-06-15T10:59:07Z 2019-04-01 |
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Type |
Research Paper
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Identifier |
Not Available
Not Available http://krishi.icar.gov.in/jspui/handle/123456789/72568 |
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Language |
English
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Relation |
Not Available;
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Publisher |
Taylor & Francis
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