Mutant mouse models and their contribution to our knowledge of corpus luteum development, function and regression

Henkes, Luiz E; Davis, John S; Rueda, Bo R

doi:10.1186/1477-7827-1-87

Reproductive Biology and Endocrinology

Table 1 Summary of Reproductive Female Phenotypes in Mutant Mice models.

From: Mutant mouse models and their contribution to our knowledge of corpus luteum development, function and regression

Mutant mice models with preovulatory/luteal development defects/anomalies
MUTANT	REPRODUCTIVE PHENOTYPE	REF
^aCDK2	Infertile – Follicle arrest with granulosa luteinization; Gigantism with multi tissue hyperplasia and benign adenomas in the pituitary	[16, 78]
^bCDK4	Impaired postovulatory progesterone secretion and disruption of implantation	[12, 47, 48]
^cp27^kip	Ovulation defect; granulosa cells continue to proliferate after luteinization	[46]
^dPDE4D	Infertile – Follicles with entrapped oocytes that undergo luteinization	[17]
^eNrip1	Infertile – Unruptured follicles; granulosa cells undergo luteinization	[18]
^fCon-37	Infertile – Mature oocytes fail to ovulate	[19]
^gPRLR	Infertile – Fewer follicles, reduced ovulation, irregular cycles, reduced fertilization rates, defective preimplantation embryo development an lack the ability to initiate pseudopregnancy	[54]
^hPRKO	Infertile – Inability to ovulate, uterine hyperplasia, limited mammary development and inability to exhibit sexual behavior	[11, 22, 23]
ⁱαERKO	αERKO females are acyclic, infertile and display enlarged, hemorrhagic cystic follicles with a high incidence of ovarian tumors	[9, 10, 30]
^jβERKO	βERKO females are sub fertile, have decreased ovulation rates, fewer litters, less pups and sparse corpora lutea	[10, 30, 79]
^kLHR	Infertile – arrested follicular development at the early antral stage	[38–40, 80]
^lLats – 1	Infertile-Growth retardation and lack of mammary development; Most follicles are primary and secondary; No evidence of corpora lutea formation	[43]
^mC/EBPβ	Infertile – Fail to initiate or maintain a pregnancy	[42]
ⁿeNOS	Irregular estrous cycle and reduced ovulation rate	[20, 21]
Mutant mice models with reduced luteal function
MUTANT	REPRODUCTIVE PHENOTYPE	REF
^oHyt	Infertile – Continuous diestrous	[50]
^pTIMP-1	Corpora lutea develop/sub-optimal progesterone	[51]
Mutant mice models with delayed or disrupted luteal regression
MUTANT	REPRODUCTIVE PHENOTYPE	REF
^qFP	No regression of corpora lutea and fail to spontaneusly undergo parturition	[59, 60]
^rCOX-1	Delayed parturition	[57, 58]
^sCOX-2	Reduced ovulation rates, reduced fertilization rates, implantation and decidualization defects	[15]
^tlpr	Irregular follicular development/corpora lutea undergo luteolysis at irregular intervals	[71]
^ugld	Irregular follicular development/corpora lutea undergo luteolysis at irregular intervals	[71]
^vTNFR	Increased number of ovulations, irregular estrous cycles, eventually get locked into a diestrous phase	[67]
^wCasp3	Delayed structural luteal regression, independent of decrease in progesterone	[76, 77]
^xInsl3	Disrupted cycle length and increased ovarian apoptosis including follicles and corpora lutea	[64]

List of acronyms or abbreviations: ^aCyclin dependent kinase 2, ^bCyclin dependent kinase 4, ^cp27(kip), ^dType 4 cAMP-specific phosphodiesterase, ^eNuclear receptor co-repressor Nrip1 (a.k.a. RIP140), ^fConnexin-37, ^gProlactin receptor, ^hProgesterone receptor, ⁱαEstrogen receptor, ^jβEstrogen receptor, ^kLuteinizing hormone receptor, ^lLarge tumor suppressor homolog 1, ^mCCAAT/enhancer-binding protein β, ⁿEndothelial nitric oxide synthase, ^oHypothyroid, ^pTissue inhibitor of metalloproteinase-1, ^qProstaglandin F2α receptor, ^rCyclooxygenase-1, ^sCyclooxygenase-2, ^tlymphoproliferation, ^ugeneralized lymphoproliferative disease, ^vTumor necrosis factor receptor, ^wCaspase-3, ^xInsulin-like factor 3

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ISSN: 1477-7827

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