Animal reproduction Question 1: Hormone action of a lipo- soluble hormone A.

My structure is progesterone (P4) and its function is to form secretion glands in endometrium. B1. Inserting CIDR (intravaginal p4 insert) in cow would result in formation in endometrium secretion glands. This could be observed under microscope if sample is taken out of cow endometrium. B2. If moderate amount of p4 antagonist is introduced in the cow it would result in decreased in secretion gland formation. B3. If P4 level destroyed by introducing PGF2 (intravaginal insert) then, no secretion glands would observed in the endometrium. C1. The level of organization is micro. C2. P4 produced from CL travels to uterus by binding to serum globulin. At this target cell it diffuses through the cell membrane leaving transfer protein behind and binds with specific p4 receptor. This hormone-receptor complex forms dimer with cofactors and binds the specific promoter region on the DNA. RNA POL2 also binds here and this complex transcribes specific genes. mRNA goes out through nuclear pore and gets translated through ribosomes. The translated protein will modify in the Golgi complex and result as a secretion gland. C3. Secretion glands created by p4 prepares endometrium for fertilization and also secretes other hormone like pgf2 which would inhibit p4 and endometrium if no fertilization occurs and prepares female for next cycle. This ensures reproductive success. D1. Pgf2 created from endometrium would inhibit secretion of p4. Oxytocin would inhibit secretion of p4 by killing CL. D2. pgf2 secreted from endometrium binds to serum globulin in the blood and diffuses from UOV to OA by counter current exchange. On the OA, pgf2 binds to pgf2 receptor on the surface membrane. This would open the Ca++ channel. Influx of Ca2+ would cause vasoconstriction. This would lead to poor blood flow in the CL. This would result in Apoptosis of CL. Which would stop inhibit p4. D3. My hormone is pgf2 and its receptor is pgf2 receptor.

Q2. Hormone action of water soluble hormone A. My structure is FSH and its function is to produce inhibin. B1. (In order for experiment to keep in the follicular phase pgf2a is introduced before performing experiment) inject high level of FSH it would result in high level of inhibin. EISA could be performed to see the result. B2 lowering FSH level with moderate amount of antagonistic drug would result in low level of inhibin B3. Destroying anterior pituitary of pig would show negative result for inhibin in Elisa. C1. The level of organization is micro C2. FSH released from Anterior Pituitary (AP) travels to follicles in the ovary via blood and binds to FSH receptor on the cell surface of the granulosa cell. This would cause G protein to attach with membrane bound enzyme Adenyl cyclase. This convers ATP in to cAMP, cAMP serves as a 2nd messanger and binds to regulatory subunit of protein kinase which activates catalytic subunit. This binds to CREB, and CREB will bind CRE on the promoter. This will transcribe mRNA which will go out of the nucleus though pore and will get translated by ribosome. This translated protein is inhibin. C3. Inhibin as it name sounds inhibits FSH production in female causing preovulatory LH surge. this is important for the ovulation to occur. D1. Inhibin inhibits p4. E2 inhibits p4. D2. Inhibin produced from follicles travel in blood to the anterior pituitary. It binds to specific inhibin surface receptor. This would cause G protein to attach with membrane bound enzyme Adenyl cyclase. This convers ATP in to cAMP, cAMP serves as a 2nd messanger and binds to regulatory subunit of protein kinase which activates catalytic subunit. This binds to CREB, and CREB will bind CRE on the promoter. This would stop transcription of FSH. D3. My hormone is FSH and the receptor is FSH receptor.

Q3. The hypothalamic pituitary unit A. My structure is GnRH neuron complex and its function is to provide preovulatory E2. B1. Increasing AP in GnRH neuron w/ electrode will show high E2 and show shorter follicular phase in cow B2.Destroying GnRH Neurons in Cow would result in no preovulatory E2 B3. Slowing ap in GnRH neuron would cause longer follicular phase in cow C1. The level of organization is micro. C2. GnRh neuron complex located in tonic center stimulates AP which causes release of GnRH in to the primary portal plexus in the anterior pituitary via neuron terminal. `gnrh binds to gnrh receptors on the surface membrane of anterior pituitary. This would cause G protein to attach with membrane bound enzyme Adenyl cyclase. This convers ATP in to cAMP, cAMP serves as a 2nd messanger and binds to regulatory subunit of protein kinase which activates catalytic subunit. This binds to CREB, and CREB will bind CRE on the promoter. Specific genes get transcribed. mRNA will go out from nuclear pores and will get transcribe through ribosomes. This would produce LH and FSH. These hormones would trigger follicular growth LH would produce Androgen via theca cell and FSH will aromatise and turn it in to E2. C3. The production of E2 causes LH surge which causes ovulation which can be fertilized if sperm is introduced. D1. E2 is negative feedback to tonic center by stopping E2 production. Inhibin plays role in negative feedback of E2. D2. E2 produced from the follicle binds to intranuclear E2 receptors in tonic center GnRH neuron which will make dimer with the cofactor and attach to promoter region. RNA POL2 will attach with them and will transcribe the gene which inhibits GnRH. Inhibition of GnRH will also inhibit gonadotropins which would cause follicles to not grow resulting in inhibition of E2. D3. My structure is E2 and the receptor is E2 receptor.

Q4. Control of the onset on puberty A. My structure is GnRH and its fuction is to proliferate LH onset puberty. B1. Increase in GnRH would cause increase in LH comparing prepubertal and onset puberty B2. Increase in GnRH would cause increase in PKA by ELISA B3. Blocking GnRH neuron with antagonist would stop producing LH for that limited time C1. The level of organization is micro. C2. GnRH stimulated from hypothalamus binds to GnRh neurons on the surface of AP cell. It will cause G protein to bind with membrane bound enzyme AC. AC turns ATP in to cAMP, this acts as 2nd messanger and bins to PKA activating catalytic subunit. Catalytic subunit would bind to CREB. this would then bind to CRE on the promoter region transcribing mRNA. mRNA will move out of nucleus and will get translated via ribosome increasing LH. C3. Increase in LH would cause LH surge in female and thus menstrual cycle continues in female. In males proliferated LH would cause increase in testosterone. D1. P4 would inhibit GnRH. P4 would also inhibit LH D2. P4 produced from CL travels to uterus by binding to serum globulin. At this target cell it diffuses through the cell membrane leaving transfer protein behind and binds with specific p4 receptor. This hormone-receptor complex forms dimer with cofactors and binds the specific promoter region on the DNA. RNA POL2 also binds here and this complex stops transcribing LH genes. This will cause inhibition of LH. D3. My hormone is p4 and its receptor is p4 receptor.

Q5. The endocrinology of the follicular phase A. My structure is FSH and its function is to produce E2. B1.Increase in FSH increasein E2 in vivo with follicle present B2.decrease in FSH will decrease in E2 in vivo B3. NO FSH and just follicle would not produce E2 in vivo C1. The level of organization is micro. C2. FSH produced from anterior pituitary travels to the ovaries via blood. FSH binds FSH receptor on the surface of granulosa cells. Binding of hormone receptor activated G protein. It binds to AC on the membrane. It would turn ATP in to cAMP. cAMP acts as 2nd messanger and will bind to protein kinase activating catalytic unit. This will bind to transcription factor CREB. CREB binds on CRE on the promoter and transcribes mRNA. mRNA will go out of the nucleus and get transcribed producing aromatase then will convert testosterone produce from theca cell into E2. C3. E2 created by FSH in follicular phase causes LH surge which then causes ovulation. Ovulation is necessary for reproduction. D1. E2 causes inhibition of FSH Inhibin causes inhibition of FSH. D2. E2 produced in the ovaries travel to cells in anterior pituitary by binding with serum globulin via blood. It diffuses in to the cell membrane and binds to its E2 receptor. Hormome and receptor complex makes dimer with cofactors. This will attach to promoter region on the DNA and with help of RNA POL2 gene transcription of FSH suppresses. D3. My hormone is E2 and its receptor is E2 receptor.

Q6. The endocrinology of the luteal phase A. My structure is LH surge and its function is to produce P4 during luteal phase. B1. Using RIA hormone leves are checked, P4 peaks high after High LH peak is extreme B2 Before LH surge p4 level is showed to be low B3. Blocking LH surge caused destroyed p4 C1. The level of organization is micro. C2. LH surge produced from anterior pituitary travels to the target cells in CL via blood. It binds to LH receptor on the surface. This activates the G protein. It would bind to Adenyl cyclase. AC will convert ATP in to cAMP. cAMP serves as 2nd messanger. Binds to PKA, PKB, and PKC and will activate three different catalytic subunits a, b, and c. a will accelerate LDL- cholesterol receptors, b produces enzyme cholesterols binding with CREB. This separates cholesterol from ester and c promotes entry of cholesterol in the mitochondria. That transfers cholesterol in to preglenolone and with enzyme produced in SER it transfers in to p4. C3. P4 created by CL has multipurpose. It creates endometrium in uterus for nutritional purpose of fertilized egg. It also makes mucosa in the cervix less thicker so sperm can travel in. D1. P4 inhibits LH directly acting at anterior pituitary and p4 could inhibit LH inhibiting GnRH. D2. P4 produced from CL travels to uterus by binding to serum globulin. At this target cell it diffuses through the cell membrane leaving transfer protein behind and binds with specific p4 receptor. This hormone-receptor complex forms dimer with cofactors and binds the specific promoter region on the DNA. RNA POL2 also binds here and this complex stops transcribing LH genes. This will cause inhibition of LH. D3. My hormone is p4 and its receptor is p4 receptor

Q7. The endocrinology of spermatogenesis A. My structure is LH and its function is to testosterone production. B1. In male pig LH level was set to zero by destroying AP lobe testosterone production stopped using ELISA B2. Increase in LH level increased testosterone (on set puberty) B3.decresed LH level decreases testosterone (prepubertal male) C1. The level of organization is micro. C2. LH travels from anterior pituitary to ledig cells attached to testis via blood. On the ledig cells LH binds to its receptors call LH receptors. Binding of hormone receptor activated G protein. It binds to AC on the membrane. It would turn ATP in to cAMP. cAMP acts as 2nd messanger and will bind to protein kinase activating catalytic unit. This will bind to transcription factor CREB. CREB binds on CRE on the promoter and transcribes mRNA. mRNA will go out of the nucleus and get transcribed producing enzyme called side cleaving enzyme. Additional enzymes from SER will turn Cholesterol in to testosterone. C3. Production of testosterone in male insures spermatogenesis. This is essential for reproduction, D1. Testosterone inhibits GNRH then will inhibit LH P4 inhibits LH. D2. Testosterone binds to ABP created by sertoli cells and travels to the hypothalamus via blood. It diffuses through target cell membrane and binds to the Testosterone receptors in the nucleus. This receptor- hormone complex forms dimer with cofactors and which attaches to the DNA in promoter region which stops the transcription of genes producing GnRH. this would inhibit LH. D3. My hormone is Testosterone and the hormone receptor is testerone receptor.

Q8. Endocrinology of reproductive behavior A. My structure is preovulatory E2 and its function is to cause lordosis in female animal in present of male. B1. Injecting excess of E2 in cow shows increase in lordosis in present of male or female B2. Blocking E2 moderately with antagonistic drug would reduce lordosis behaviour B3. Destroying E2 by Pgf2a will cause in no lordosis C1. The level of organization is micro C2. In the present of ox sensory nerves from cow sends AP to the sexual area in the brain. Preovulatory E2 produced in antral follicle also travels to the sexual area in the brain via blood binding through serum albumin. E2 binds to intranuclear E2 receptor in this target cell. Hormone and receptor complex makes dimer with cofactors. This complex attaches to the DNA on the promoter region with the help of RNA POLY2 gene transcribes. And behavior specific peptides are translated by ribosomes. These peptides get released through post synaptic neurons in receiving zone for hypothalamic peptides. This speeds up the impulses. This impulse travels through motor neurons in the spin cord to the back muscle. These impulses opens Ca+2 channels in the back muscle causing contraction causing increase in the spinal curve and relaxing the posterior muscle. C3. Lordosis behavior of female animals are important signal for sexual receptivity during estrus. This helps female in copulation position and signals that female is ready to get pregnant. D1. P4 inhibits GnRH inhibiting LH which inhibits E2 P4 inhibits Anterior pituitary gland which then inhibits E2. D2.P4 produced from CL binds to serum albumin and travels to the target tissue in the surge center here it binds to p4 receptor in the nucleus diffusing through cell membrane. P4 and receptor complex makes dimer with cofactor. This dimer cofactor attaches to the DNA on the promoter region of DNA and stops transcribing GnRH mRNA. This causes inhibition of GnRH. This will inhibit pituitary gland to produce LH. This would result in to E2 inhibition. If LH surge is triggered thenE2 and Lordosis behavior cannot be stopped. Because it is like bullet out of the gun cant go back in once it is out that means it out. D3.Hormone is P4 and receptor is P4 recepter.

Q9. Endocrine- based technologies A. My structure is p4 and its function is to serve as contraceptive by suppressing ovulation in female. B1. Taking p4 daily pills would show no period B2.missing p4 pills would show period once in a while B3 not taking p4pills at all will continue in period C1. The level of organization is micro. C2. Contraceptive p4 binds to serum globulin and travels to the target cell in hypothalamus via blood. Hormone unbinds serum globuline once reaches to at the target cell and binds to the intraneuclar receptor by diffusing through the membrane. Hormone receptor complex travels in nucleus, makes dimer with cofactor. This attaches to DNA on the promoter region including RNAPOLY2. This stops transcription of the gnRH gene. Inhibition of GnRH will inhibit LH surge thus, no ovulation. C3. P4 as contraceptive inhibits ovulation thus resulting in no egg for fertilization.so, female can have as much sex as she wants. This would avoid pregnancy. It has to introduce therefore before LH surge. And continue dose every day because once LH surge take place that means cannot be stoppable. D1,2,3. No negative feedback to this contraceptive is known. PGF2a usually creates vasoconstriction in OA and causes apoptosis of CL but this progesterone is taken as a pill so, doesnt really have negative feedback this makes this contraceptive even better.

Q10. Rhythms, reproduction, and aging A. My structure is preovulatory E2 and its function is to proliferate LH surge B1. (After introducing pgf2a in vagina this experiment was designed just make sure we are in follicular phse) increase inE2 show increase in blood LH level quick B2. Decreased in E2 cause delay in LH surge B3. No E2 would show no LH surge C1. the level of organization is micro. C2. E2 from the Antrum diffuses through the follicles then it bings to globuline in the bloodand travel to hypothalamic surge center and binds to E2 receptor. E2 and E2 recepter complex forms dimer with cofactors and complex binds to DNA in the promoter region. It transcribes mRNA which comes out in the cytoplasm and gets translated by ribosime producing GnRH. High leve of gnRh will produce high level of GnRH will produce high level of LH. C3. LH surge is required for ovulation and transformation of granulosa and theca cells in to CL. D1, 2, 3. No negative feed back because once LH surge is triggered it can not be stopped. It is like bullet out of the gun. It will go.