Oocyte Transport

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Régis Giet - One of the best experts on this subject based on the ideXlab platform.

  • Dual control of Kinesin-1 recruitment to microtubules by Ensconsin in Drosophila neuroblasts and Oocytes
    Development (Cambridge England), 2019
    Co-Authors: Mathieu Métivier, Brigette Monroy, Emmanuel Gallaud, Renaud Caous, Aude Pascal, Laurent Richard-parpaillon, Antoine Guichet, Kassandra Ori-mckenney, Régis Giet
    Abstract:

    Drosophila Ensconsin (also known as MAP7) controls spindle length, centrosome separation in brain neuroblasts (NBs) and asymmetric Transport in Oocytes. The control of spindle length by Ensconsin is Kinesin-1 independent but centrosome separation and Oocyte Transport require targeting of Kinesin-1 to microtubules by Ensconsin. However, the molecular mechanism used for this targeting remains unclear. Ensconsin contains a microtubule (MT)-binding domain (MBD) and a Kinesin-binding domain (KBD). Rescue experiments show that only full-length Ensconsin restores the spindle length phenotype. KBD expression rescues ensc centrosome separation defects in NBs, but not the fast Oocyte streaming and the localization of Staufen and Gurken. Interestingly, the KBD can stimulate Kinesin-1 targeting to MTs in vivo and in vitro We propose that a KBD and Kinesin-1 complex is a minimal activation module that increases Kinesin-1 affinity for MTs. Addition of the MBD present in full-length Ensconsin allows this process to occur directly on the MT and triggers higher Kinesin-1 targeting. This dual regulation by Ensconsin is essential for optimal Kinesin-1 targeting to MTs in Oocytes, but not in NBs, illustrating the importance of adapting Kinesin-1 recruitment to different biological contexts.

K Hinrichs - One of the best experts on this subject based on the ideXlab platform.

  • effect of potential Oocyte Transport protocols on blastocyst rates after intracytoplasmic sperm injection in the horse
    Equine Veterinary Journal, 2013
    Co-Authors: R Foss, H Ortis, K Hinrichs
    Abstract:

    Summary Reasons for performing study Intracytoplasmic sperm injection (ICSI) is used to produce foals from otherwise infertile mares and from stallions with limited sperm stores, but requires expensive equipment and is technically demanding. Methods to Transport Oocytes to ICSI laboratories would allow collection of Oocytes by the referring veterinarian and enable greater application of this technique. Objectives This study was conducted to evaluate protocols that could be used to Transport immature and maturing Oocytes for ICSI. Study design In vitro experiment. Methods Oocytes were recovered by transvaginal ultrasound-guided follicular aspiration either from dominant follicles 24 h after deslorelin administration (dominant stimulated follicle [DSF]), or from subordinate (immature) follicles at the same time. To mimic Transport, DSF Oocytes were incubated overnight under differing conditions before ICSI; immature Oocytes were placed in varying conditions overnight before in vitro maturation, followed by ICSI. The rate of blastocyst production was compared among treatments. Results Blastocysts were produced in all groups. Dominant stimulated follicle Oocytes held in sealed tubes in pre-equilibrated control maturation medium maintained at 37°C yielded blastocyst development equal to that obtained for control incubated Oocytes (70%). Dominant stimulated follicle Oocytes held similarly in a warm passive device yielded poor blastocyst development (10%). Immature Oocytes held for one or 2 nights in modified M199 medium, or for one night in commercial embryo holding solution, in air at room temperature, yielded 35–37% blastocyst development per injected Oocyte. Conclusions A commercially available medium can be used for shipping immature Oocytes at room temperature with good resulting blastocyst rates. Better blastocyst rates per Oocyte are obtained from DSF Oocytes; however, these require maintenance at 37°C and as they are already maturing at the time of collection, are more sensitive to delays. This new, practical information supporting Transport of both immature and DSF Oocytes for ICSI may allow wider use of this procedure.

  • holding immature equine Oocytes in the absence of meiotic inhibitors effect on germinal vesicle chromatin and blastocyst development after intracytoplasmic sperm injection
    Theriogenology, 2006
    Co-Authors: Y H Choi, L B Love, D D Varner, K Hinrichs
    Abstract:

    Holding immature Oocytes before the onset of maturation simplifies Oocyte Transport and aids in scheduling later manipulations. We report here a method for holding equine Oocytes in the absence of meiotic inhibitors. In Experiment 1, immature Oocytes with expanded cumuli were cultured at 38.2 degrees C in medium containing cycloheximide, or were held at room-temperature in M199 with Hanks' salts, for 16-18 h before maturation. Control Oocytes were matured immediately after recovery. Oocytes were fertilized by intracytoplasmic sperm injection and cultured for 4d. Embryo development was not different among treatments. In Experiment 2, Oocytes were treated as in Experiment 1, but embryos were cultured for 7.5d. Blastocyst development was significantly lower in the cycloheximide-treated group than in controls (7% versus 30%) with the room-temperature group intermediate (16%). In Experiment 3, Oocytes were cultured at 38.2 degrees C in medium containing roscovitine, or were held at room temperature in sealed glass vials in a mixture of 40% M199 with Earle's salts, 40% M199 with Hanks' salts, and 20% FBS (EH treatment) for 16-18 h, before maturation, sperm injection, and embryo culture for 7.5d. Blastocyst development of Oocytes in the EH treatment was significantly higher than that for roscovitine-treated Oocytes (34% versus 12%), but not significantly different from that for controls (25%). Oocytes in the EH treatment did not mature during holding (70% germinal vesicle stage after 18 h holding). Whereas culture with cycloheximide or roscovitine of equine Oocytes with expanded cumuli reduced subsequent blastocyst formation, these Oocytes could be held in a modified M199 at room temperature overnight without adverse affecting meiotic or developmental competence.

  • effect of ovary storage and Oocyte Transport method on maturation rate of horse Oocytes
    Theriogenology, 2003
    Co-Authors: L B Love, Y H Choi, Charles C Love, D D Varner, K Hinrichs
    Abstract:

    Abstract Two experiments were conducted to determine the effects of storage on equine ovaries or isolated Oocytes. Ovaries were collected at an abattoir and were maintained at room temperature during collection and Transport (3–9 h total). After arrival at the laboratory, ovaries were divided into three groups: immediate Oocyte collection (control), storage at room temperature overnight (15–18 h) before Oocyte collection, or storage at 4 °C overnight before Oocyte collection. Collected Oocytes were cultured in maturation medium for 24 h. There was a significant increase in the proportion of Oocytes classified as having compact cumuli in the two storage groups when compared with the controls. For Oocytes originally having expanded cumuli, the rate of maturation to MII was significantly higher in the control group (72%) than in either storage group, and the maturation rate for Oocytes from ovaries stored at room temperature (27%) was significantly higher than that for ovaries stored at 4 °C (10%). A similar trend was seen for Oocytes originally having compact cumuli (24, 11, and 3% in MI–II for control, room temperature, and cold groups, respectively). In Experiment 2, we evaluated the effect of different packaging systems on the maturation of horse Oocytes within a portable incubator. Use of 1 ml of equilibrated maturation medium in a 1 ml glass vial was associated with maturation equivalent to that for standard incubation.

Mathieu Métivier - One of the best experts on this subject based on the ideXlab platform.

  • Dual control of Kinesin-1 recruitment to microtubules by Ensconsin in Drosophila neuroblasts and Oocytes
    Development (Cambridge England), 2019
    Co-Authors: Mathieu Métivier, Brigette Monroy, Emmanuel Gallaud, Renaud Caous, Aude Pascal, Laurent Richard-parpaillon, Antoine Guichet, Kassandra Ori-mckenney, Régis Giet
    Abstract:

    Drosophila Ensconsin (also known as MAP7) controls spindle length, centrosome separation in brain neuroblasts (NBs) and asymmetric Transport in Oocytes. The control of spindle length by Ensconsin is Kinesin-1 independent but centrosome separation and Oocyte Transport require targeting of Kinesin-1 to microtubules by Ensconsin. However, the molecular mechanism used for this targeting remains unclear. Ensconsin contains a microtubule (MT)-binding domain (MBD) and a Kinesin-binding domain (KBD). Rescue experiments show that only full-length Ensconsin restores the spindle length phenotype. KBD expression rescues ensc centrosome separation defects in NBs, but not the fast Oocyte streaming and the localization of Staufen and Gurken. Interestingly, the KBD can stimulate Kinesin-1 targeting to MTs in vivo and in vitro We propose that a KBD and Kinesin-1 complex is a minimal activation module that increases Kinesin-1 affinity for MTs. Addition of the MBD present in full-length Ensconsin allows this process to occur directly on the MT and triggers higher Kinesin-1 targeting. This dual regulation by Ensconsin is essential for optimal Kinesin-1 targeting to MTs in Oocytes, but not in NBs, illustrating the importance of adapting Kinesin-1 recruitment to different biological contexts.

Joël Henry - One of the best experts on this subject based on the ideXlab platform.

  • The SepOvotropin: A New Ovarian Peptide Regulating Oocyte Transport in Sepia officinalis
    Biochemical and Biophysical Research Communications, 2000
    Co-Authors: Céline Zatylny-gaudin, Eve Boucaud-camou, Jean Gagnon, Joël Henry
    Abstract:

    In the cuttlefish Sepia officinalis, the successive steps of egg laying are controlled by multiple neuropeptides. Recent experiments led us to suppose that there was possible involvement of a second regulation pathway by the release of ovarian regulatory peptides in the genital tract. Using HPLC fractionation and an in vitro biological test, a C-terminal amidated peptide modulating the motility of the Sepia officinalis oviduct was isolated from an extract of vitellogenic ovarian follicles. The mass of this peptide as determined by MALDI-TOF (1501.8 Da) and analysis by Edman degradation led to the following sequence: Pro-Lys-Asp-Ser-Met-Leu-Leu-Leu-Gln-Val-Pro-Val-Tyr-amide. The peptide mapping performed by LC/MS revealed a distribution restricted to the follicles, the full grown Oocytes and the eggs. This new peptide, called SepOvotropin, modulated contractions of the whole genital tract in physiological conditions from a threshold concentration between 10(-20) and 10(-19) M, demonstrating for the first time the occurrence of a specific peptidergic control of egg-laying in cephalopods.

Sean M. Ward - One of the best experts on this subject based on the ideXlab platform.

  • electrical slow waves in the mouse oviduct are dependent upon a calcium activated chloride conductance encoded by tmem16a
    Biology of Reproduction, 2012
    Co-Authors: Rose E. Dixon, Grant W. Hennig, Kenton M. Sanders, Salah A Baker, Fiona C Britton, Brian D Harfe, Jason R Rock, Sean M. Ward
    Abstract:

    Myosalpinx contractions are critical for Oocyte Transport along the oviduct. A specialized population of pacemaker cells—oviduct interstitial cells of Cajal—generate slow waves, the electrical events underlying myosalpinx contractions. The ionic basis of oviduct pacemaker activity is unknown. We examined the role of a new class of Ca2+-activated Cl− channels (CaCCs)—anoctamin 1, encoded by Tmem16a—in oviduct slow wave generation. RT-PCR revealed the transcriptional expression of Tmem16a-encoded CaCCs in the myosalpinx. Intracellular microelectrode recordings were performed in the presence of two pharmacologically distinct Cl− channel antagonists, anthracene-9-carboxylic acid and niflumic acid. Both of these inhibitors caused membrane hyperpolarization, reduced the duration of slow waves, and ultimately inhibited pacemaker activity. Niflumic acid also inhibited propagating calcium waves within the myosalpinx. Slow waves were present at birth in wild-type and heterozygous oviducts but failed to develop by birth in mice homozygous for a null allele of Tmem16a (Tmem16atm1Bdh/tm1Bdh). These data suggest that Tmem16a-encoded CaCCs contribute to membrane potential and are responsible for the upstroke and plateau phases of oviduct slow waves.

  • Chlamydia Infection Causes Loss of Pacemaker Cells and Inhibits Oocyte Transport in the Mouse Oviduct
    Biology of reproduction, 2008
    Co-Authors: Rose E. Dixon, Sung Jin Hwang, Grant W. Hennig, Kyle H. Ramsey, Justin H. Schripsema, Kenton M. Sanders, Sean M. Ward
    Abstract:

    Chlamydia trachomatis is a common sexually transmitted bacterial infection that results in health care costs in the United States that exceed $2 billion per year. Chlamydia infections cause damage to the oviducts, resulting in ectopic pregnancy and tubal factor infertility, but the reasons for defective oviduct function are poorly understood. We have investigated the role of oviduct contractions in egg Transport and found that underlying electrical pacemaker activity is responsible for oviduct motility and egg Transport. Specialized pacemaker cells, referred to as oviduct interstitial cells of Cajal (ICC-OVI), are responsible for pacemaker activity. The ICC-OVI, labeled with antibodies to KIT protein, form a dense network associated with the smooth muscle cells along the entire length of the oviduct. Selective removal of ICC-OVI with KIT-neutralizing antibody resulted in loss of electrical rhythmicity and loss of propulsive contractions of the oviduct. We tested whether infection might adversely affect the ICC-OVI. Mice infected with Chlamydia muridarum displayed dilation of oviducts, pyosalpinx, and loss of spontaneous contractile activity. Morphological inspection showed disruption of ICC-OVI networks, and electrophysiological recordings showed loss of intrinsic pacemaker activity without change in basal smooth muscle membrane potential. Chlamydia infection also was associated with upregulation of NOS2 (iNOS) and PTGS2 (COX II) in leukocytes. Loss of ICC-OVI and pacemaker activity causes oviduct pseudo-obstruction and loss of propulsive contractions for Oocytes. This, accompanied by retention of oviduct secretions, may contribute to the development of tubal factor infertility.