Molecular Reproduction and Development最新文献

This manuscript was originally written in German by one of the founding members of the field of spermatogenesis, Dr. Adolph von La Valette-St. George. Published in 1865, this important work carefully described, using samples from a wide variety of vertebrate species, essential aspects of male germ cells including the acrosome, the residual body of shed excess spermatid cytoplasm, and the flagellum. In addition, he correctly deduced that sperm formed from precursor germ cells rather than somatic cells and that their motility was due to movement of the flagellum. Here, we present an English translation and modern interpretation of one of Dr. La Valette-St. George's most important contributions from his lengthy productive academic career.

c-Abl encodes a cytoplasmic and nuclear protein tyrosine kinase that has been implicated in processes of cell growth, proliferation, differentiation, division, and regulation of cytoskeletal structure. mTERT is a catalytic subunit of mouse telomerase and it is very important for controlling cell proliferation and homeostasis by maintaining telomere length. We demonstrated before the interaction between c-Abl and mTERT in mouse ovary and we suggested a role for c-Abl in the regulation of telomerase function and proliferation in mouse granulosa cells. The current study aims to examine the c-Abl and mTERT expression and potential interactions through mouse preimplantation embryonic development. To assess c-Abl's function in embryonic development, siRNA-mediated silencing of the c-Abl was used in mouse preimplantation embryos. After siRNA transfection, the immunofluorescence was used to examine the c-Abl pattern at embryonic development. Next, the levels of mTERT and c-Abl mRNA were compared. The results show that c-Abl is expressed in mouse preimplantation embryos at all developmental stages, with the cytoplasmic expression all through from the 2-cell to the blastocyst. Additionally, c-Abl is presented very intense expression in blastomer-blastomer junctions. The siRNA-mediated depletion of c-Abl showed developmental abnormalities at the 8- to 16-cell and morula to blastocyst and also with significantly decreased blastocyst development rate. Moreover, expression of the mTERT telomerase catalytic subunit was significantly reduced in c-Abl-depleted embryos during preimplantation embryonic development. Finally, we demonstrate that c-Abl may play a crucial role in compaction and preimplantation embryo development, and that the relationship between c-Abl and mTERT has developmental importance in early embryogenesis.

This study assessed transcriptional changes in human cumulus cells (CCs) during oocyte maturation In Vitro. CCs were collected from 25 cumulus-oocyte complexes derived from surplus ovarian medulla tissue of eight women (mean age 29 years, range 19–36) undergoing ovarian tissue cryopreservation without ovarian stimulation. Samples included CCs from fresh germinal vesicle (GV) oocytes (n = 5), and from GV (n = 8) and metaphase II (MII) oocytes (n = 12) after 48 h of In Vitro maturation (IVM). Microarray analysis revealed active signaling pathways during IVM, emphasizing LHCGR upregulation as central to oocyte maturation. Enhanced pathways included the insulin-like growth factor (IGF) system, particularly IGF2, and activin/inhibin signaling, while others appeared less active In Vitro compared to In Vivo. Differential expression analysis identified 1763 significantly expressed genes (DEGs) between fresh GV and MII-IVM, 50 DEGs between GV-IVM and MII-IVM, and 339 novel or unknown transcripts. Clustering highlighted additional pathways, such as MAPK, PPAR, Wnt, cholesterol metabolism, PI3K-AKT, TGF-β, focal adhesion, actin cytoskeleton regulation, and RANK/RANKL, with differential regulation during IVM. These findings underscore the complexity of signaling in CCs and the distinct regulatory mechanisms of human oocyte maturation In Vitro compared to In Vivo.

Kaupp, U. B. and O. Kendall. 2024. “David Garbers' Contributions to Chemotaxis Signaling in Sperm.” Molecular Reproduction and Development 91: e23774. https://doi.org/10.1002/mrd.23774

The authors note that it came to their attention that Dr. HC Lee did not join David Garber's laboratory, as stated in the article. Instead, Dr. Lee, then at the University of Minnesota, collaborated with Dr. Garbers on the properties of Na/H exchange.

We apologize for this error.

Meiosis is a fundamental aspect of gametogenesis, but how and when the programming is established in germ cells during development is unknown. In the mammalian male germline, mitotic differentiating spermatogonia with the competence for meiotic divisions arise from an undifferentiated pool of spermatogonia that are descended from prospermatogonial precursors. Here we provide evidence from mouse models that suggests programming for meiotic competence is established much earlier in the developmental trajectory of spermatogonia than previously believed, likely at the prospermatogonial stage in fetal life. Conditional overexpression of the gene Id4 in prospermatogonia led to a block in meiotic progression of spermatocytes during postnatal spermatogenesis. In contrast, meiotic progression was found to proceed when Id4 was conditionally overexpressed beginning in postnatal spermatogonia. Moreover, conditional overexpression of Id4 in the female germline beginning at the fetal stage of development after oocytes have initiated meiosis did not disrupt their ability to progress postnatally. Collectively, these findings suggest that a new stage for where mechanistic insights into the origin of meiotic competence in the male germline should be explored. Moreover, the findings place further precedence on defining how outside exposures can disrupt programming at the earliest stages of male germ cell development that will manifest at advanced maturation stages and lead to genomic abnormalities.

Epigenetic changes caused by methylphenidate hydrochloride on paternal inheritance have been suggested in fish, yet a subject to be determined in mammals. In rats, we showed increased sperm DNA fragmentation and reduced embryonic viability. In the present report, male Wistar rats (n = 21) were divided into two groups: control and methylphenidate. The control group received 1 mL/kg of distilled water, while the methylphenidate group received 5 mg/kg by gavage from 38 to 68 days of age on a single daily dose. After this period, there was an interval before exposed rats started a mating schedule with untreated/normally cycling females. Morphological quality and key epigenetic marks in the blastocysts were assessed. Immunocytochemistry was performed in fresh blastocysts to quantify the trimethylated histones H3K4, H3K9, and H4K20. Treatment with methylphenidate reduced the mean quality of blastocysts by 43.57% (p = 0.02), as well as increased those classified as “poor” by more than 150% (p < 0.001). Epigenetic marks were also altered, with an increase in the intensity of H3K9me3 (p = 0.01), a reduction of H4K20me3 (p = 0.05) and a nonsignificant increase of H3K4me3 (p = 0.34). The results suggest that the decline in blastocyst quality is highly associated with subchronic use of this psychostimulant by adolescent males. This is the first report showing the risks posed by methylphenidate to the epigenetic signature of a mammalian blastocyst following paternal exposure.