During sexual reproduction or conjugation, ciliates form a specialized cell adhesion zone for the purpose of exchanging gametic pronuclei. Hundreds of individual membrane fusion events transform the adhesion zone into a perforated membrane curtain, the mating junction. Pronuclei from each mating partner are propelled through this fenestrated membrane junction by a web of short, cris-crossing microtubules. Pronuclear passage results in the formation of two breaches in the membrane junction. Following pronuclear exchange and karyogamy (fertilization), cells seal these twin membrane breaches thereby re-establishing cellular independence. This would seem like a straightforward problem: simply grow membrane in from the edges of each breach in a fashion similar to how animal cells "grow" their cytokinetic furrows or how plant cells construct a cell wall during mitosis. Serial section electron microscopy and 3-D electron tomography reveal that the actual mechanism is less straightforward. Each of the two membrane breaches transforms into a bowed membrane assembly platform. The resulting membrane protrusions continue to grow into the cytoplasm of the mating partner, traverse the cytoplasm in anti-parallel directions and make contact with the plasma membrane that flanks the mating junction. This investigation reveals the details of a novel, developmentally-induced mechanism of membrane disruption and restoration associated with pronuclear exchange and fertilization in the ciliate, Tetrahymena thermophila.
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http://dx.doi.org/10.1016/j.ydbio.2018.09.019 | DOI Listing |
Theriogenology
March 2024
Cukurova University Faculty of Medicine, Departments of Physiology, Balcali, 01330, Adana, Turkey. Electronic address:
Regulation of intracellular pH (pH) is an important homeostatic function of cells. There are three major pH regulatory mechanisms: the HCO/Cl exchanger (AE), which alleviates alkalosis, and the Na/H exchanger (NHE) and Na,HCO/Cl exchanger (NDBCE), both of which counteract acidosis. NHE activity, which is high at the germinal vesicle stage of oocyte, is inhibited during meiotic maturation, while this inhibition is abolished when the oocyte reaches the pronuclear (PN) stage of the zygote.
View Article and Find Full Text PDFDiabetes
January 2024
Division of Human Genetics, Cincinnati Children's Hospital Medical Center, Cincinnati, OH.
Unlabelled: Mitochondria, the organelles responsible for generating ATP in eukaryotic cells, have been previously implicated as a contributor to diabetes. However, mitochondrial proteins are encoded by both nuclear DNA (nDNA) and mtDNA. In order to better understand the relative contribution of each of these genomes to diabetes, a chimeric mitochondrial-nuclear exchange (MNX) mouse was created via pronuclear transfer carrying nDNA from a strain susceptible to type 1 diabetes (NOD/ShiLtJ) and mtDNA from nondiabetic C57BL/6J mice.
View Article and Find Full Text PDFBiol Open
December 2021
Zoology Department, University of Oxford, 11a Mansfield Road, Oxford, OX1 3SZ, UK.
Mouse zygote morphokinetics were measured during interphase, the mitotic period, cytokinesis, and two-cell stage. Sequences of rounder-distorted-rounder shapes were revealed, as were changing patterns of cross section area. A calcium chelator and an actin-disrupting agent inhibited the area changes that occurred between pronuclear envelope breakdown and cytokinesis.
View Article and Find Full Text PDFAm J Physiol Endocrinol Metab
October 2021
Division of Molecular and Cellular Pathology, Department of Pathology, University of Alabama at Birmingham, Birmingham, Alabama.
The regulation of euglycemia is essential for human health with both chronic hypoglycemia and hyperglycemia having detrimental effects. It is well documented that the incidence of type 2 diabetes increases with age and exhibits racial disparity. Interestingly, mitochondrial DNA (mtDNA) damage also accumulates with age and its sequence varies with geographic maternal origins (maternal race).
View Article and Find Full Text PDFCell Biochem Funct
March 2021
Fertility Preservation Lab, Reproductive Medicine Center, Guangdong Second Provincial General Hospital, Guangzhou, China.
Oocyte activation deficiency leads to female infertility. [Ca ] oscillations are required for mitochondrial energy supplement transition from the resting to the excited state, but the underlying mechanisms are still very little known. Three mitochondrial Ca channels, Mitochondria Calcium Uniporter (MCU), Na /Ca Exchanger (NCLX) and Voltage-dependent Ca Channel (VDAC), were deactivated by inhibitors RU360, CGP37157 and Erastin, respectively.
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