In humans, all but 1% of monosomy 45.X embryos die in utero and those who reach term suffer from congenital abnormalities and infertility termed Turner's syndrome (TS). By contrast, XO female mice on various genetic backgrounds show much milder physical defects and normal fertility, diminishing their value as an animal model for studying the infertility of TS patients. In this article, we report that XO mice on the C57BL/6J (B6) genetic background showed early oocyte loss, infertility or subfertility and high embryonic lethality, suggesting that the effect of monosomy X in the female germline may be shared between mice and humans. First, we generated XO mice on either a mixed N2(C3H.B6) or B6 genetic background and compared the number of oocytes in neonatal ovaries; N2.XO females retained 45% of the number of oocytes in N2.XX females, whereas B6.XO females retained only 15% of that in B6.XX females. Second, while N2.XO females were as fertile as N2.XX females, both the frequency of delivery and the total number of pups delivered by B6.XO females were significantly lower than those by B6.XX females. Third, after mating with B6 males, both N2.XO and B6.XO females rarely produced XO pups carrying paternal X chromosomes, although a larger percentage of embryos was found to be XO before implantation. Furthermore, B6.XO females delivered 20% XO pups among female progeny after mating with C3H males. We conclude that the impact of monosomy X on female mouse fertility depends on the genetic background.

Premature ovarian insufficiency in the XO female mouse on the C57BL/6J genetic background.

Whole-Genome Re-sequencing and Transcriptome Reveal Candidate Genes and Pathways Associated with Hybrid Sterility in Hermaphroditic Argopecten Scallops.

Like Sand Through The Hourglass

Temperature is a critical factor affecting the growth, development and reproduction of aquatic organisms. The interspecific F1 hybrids between hermaphroditic bay scallops (Argopecten irradians) and Peruvian scallops (Argopecten purpuratus) exhibited significant heterosis in yield, but sterility in most hybrids hindered large scale interspecific hybridization and speciation. We first explored the physiological effect of temperature on the fertility of hybrid hermaphroditic Argopecten scallops with F1 hybrids treated at 6 different temperatures (18 °C, 20 °C, 22 °C, 24 °C, 26 °C, and 28 °C). The results showed that the final mortality rates from 18 °C to 22 °C were significantly lower than those from 24 °C to 28 °C. With the decrease of the temperature, the size, gonadal index, ATP content, and expression of most genes related to fertility regulation gradually decreased in F1 hybrids treated at 22 °C, 20 °C and 18 °C, and the apoptosis rate of oocytes gradually increased, but the activity of SOD (superoxide dismutase) and CAT (catalase) first increased and then decreased. The fertility of hybrids treated at 22 °C, 20 °C and 18 °C gradually decreased with the decrease of the temperature. According to gene expression, temperature may regulate the fertility of Argopecten F1 hybrids by affecting apoptosis, meiosis, ATP production and damage repair to inhibit the genesis and maturation of germ cells. Our findings suggest that temperature can affect the hybrid fertility of hermaphroditic Argopecten scallops and provide the basis for further research on the mechanism of temperature on sterility. 

Effects of temperature on fertility in hybrid hermaphroditic Argopecten scallops

The mammalian ovary is a unique organ that displays a distinctive feature of cyclic changes throughout the entire reproductive period. The estrous/menstrual cycles are associated with drastic functional and morphological rearrangements of ovarian tissue, including follicular development and degeneration, and the formation and subsequent atrophy of the corpus luteum. The flawless execution of these reiterative processes is impossible without the involvement of programmed cell death (PCD).PCD is crucial for efficient and careful clearance of excessive, depleted, or obsolete ovarian structures for ovarian cycling. Moreover, PCD facilitates selection of high-quality oocytes and formation of the ovarian reserve during embryonic and juvenile development. Disruption of PCD regulation can heavily impact the ovarian functions and is associated with various pathologies, from a moderate decrease in fertility to severe hormonal disturbance, complete loss of reproductive function, and tumorigenesis. This comprehensive review aims to provide updated information on the role of PCD in various processes occurring in normal and pathologic ovaries. Three major events of PCD in the ovary-progenitor germ cell depletion, follicular atresia, and corpus luteum degradation-are described, alongside the detailed information on molecular regulation of these processes, highlighting the contribution of apoptosis, autophagy, necroptosis, and ferroptosis. Ultimately, the current knowledge of PCD aberrations associated with pathologies, such as polycystic ovarian syndrome, premature ovarian insufficiency, and tumors of ovarian origin, is outlined.PCD is an essential element in ovarian development, functions and pathologies. A thorough understanding of molecular mechanisms regulating PCD events is required for future advances in the diagnosis and management of various disorders of the ovary and the female reproductive system in general. 

A matter of new life and cell death: programmed cell death in the mammalian ovary

Mammalian female fertility is limited by the number and quality of oocytes in the ovarian reserve. The number of oocytes is finite since all germ cells cease proliferation to become oocytes in fetal life. Moreover, 70-80% of the initial oocyte population is eliminated during fetal and neonatal development, restricting the ovarian reserve. Why so many oocytes are lost during normal development remains an enigma. In Meiotic Prophase I (MPI), oocytes go through homologous chromosome synapsis and recombination, dependent on formation and subsequent repair of DNA double strand breaks (DSBs). The oocytes that have failed in DSB repair or synapsis get eliminated mainly in neonatal ovaries. However, a large oocyte population is eliminated before birth, and the cause or mechanism of this early oocyte loss is not well understood. In the current paper, we show that the oocyte loss in fetal ovaries was prevented by a deficiency of Caspase 9 (CASP9), which is the hub of the mitochondrial apoptotic pathway. Furthermore, CASP9 and its downstream effector Caspase 3 were counteracted by endogenous X-linked Inhibitor of Apoptosis (XIAP) to regulate the oocyte population; while XIAP overexpression mimicked CASP9 deficiency, XIAP deficiency accelerated oocyte loss. In the CASP9 deficiency, more oocytes were accumulated at the pachytene stage with multiple γH2AFX foci and high LINE1 expression levels, but with normal levels of synapsis and overall DSB repair. We conclude that the oocytes with LINE1 overexpression were preferentially eliminated by CASP9-dependent apoptosis in balance with XIAP during fetal ovarian development. When such oocytes were retained, however, they get eliminated by a CASP9-independent mechanism during neonatal development. Thus, the oocyte is equipped with multiple surveillance mechanisms during MPI progression to safe-guard the quality of oocytes in the ovarian reserve.

/pdf/interplay-between-caspase-9-and-x-linked-inhibitor-of-4o1c3w7rta.pdf

Interplay between Caspase 9 and X-linked Inhibitor of Apoptosis Protein (XIAP) in the oocyte elimination during fetal mouse development.

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Interplay between Caspase 9 and X-linked Inhibitor of Apoptosis Protein (XIAP) in the oocyte elimination during fetal mouse development.