scholarly journals Defects in mating behavior are the primary cause of sterility in C. elegans males at elevated temperature

2019 ◽  
Author(s):  
Emily M. Nett ◽  
Nicholas B. Sepulveda ◽  
Lisa N. Petrella
Keyword(s):  
Elevated Temperature ◽  
Mating Behavior ◽  
Male Fertility ◽  
Male Reproduction ◽  
Temperature Sensitive ◽  
Male Mating ◽  
Sperm Activation ◽  
Successful Mating ◽  
C Elegans ◽  
Almost All

AbstractReproduction is a fundamental imperative of all forms of life. For all the advantages sexual reproduction confers, it has a deeply conserved flaw: it is temperature sensitive. As temperatures rise, fertility decreases. Across species male fertility is particularly sensitive to elevated temperature. Previously we have shown in the model nematode worm C. elegans, that all males are fertile at 20°C but almost all males have lost fertility at 27°C. Male fertility is dependent on the production functional sperm, successful mating and transfer of sperm, and successful fertilization post-mating. To determine how male fertility is impacted by elevated temperature we analyzed these aspects of male reproduction at 27°C in three wild-type strains of C. elegans: JU1171, LKC34, and N2. We found no effect of elevated temperature on the number of immature non-motile spermatids formed. There was a weak effect of elevated temperature on sperm activation that may negatively impact sperm function. In stark contrast, there was a strong effect of elevated temperature on male mating behavior and sperm transfer such that males very rarely successfully completed mating when exposed to 27°C. Therefore, we propose a model where elevated temperature reduces male fertility due to the negative impacts of temperature on the somatic tissues necessary for mating. Loss of successful mating at elevated temperature overrides any effects that temperature may have on the germline or sperm cells.

Hypoxia and reproduction in Swiss mice

1962 ◽  
Vol 202 (4) ◽  
pp. 611-615 ◽  
Author(s):  
Bernard Baird ◽  
S. F. Cook
Keyword(s):  
Adverse Effects ◽  
Sea Level ◽  
Mating Behavior ◽  
Stress Level ◽  
Functional Impairment ◽  
Male Fertility ◽  
Critical Size ◽  
Fetal Tissue ◽  
Gestation Time ◽  
Almost All

Swiss albino mice were maintained in closed decompression chambers: 1) continuously at simulated altitudes of 14,200 and 18,000 ft; 2) intermittently, 6 hr/day, at 20,000, 21,500, and 25,000 ft; 3) continuously at sea level with atmosphere of 12% oxygen, 88% nitrogen. All animals were acclimatized before exposure. In all cases mating behavior was normal, and there was no functional impairment of male fertility. Impregnation was observed with all mated, adapted females in almost all experiments. Exceptions were considered due to early resorption of embryos. No significant effect of hypoxia was noted on implantation, placentas, vascularization, gestation time, or parturition. Adverse effects of hypoxia were manifested primarily in resorption of fetuses when they had attained a critical size (about 7 mm). The incidence of resorption correlated directly with stress level, expressed as duration and intensity of hypoxia, and is considered to be contingent on the critically respiring mass of fetal tissue.

Analysis of C. elegans acetylcholine synthesis mutants reveals a temperature-sensitive requirement for cholinergic neuromuscular function

Genetics ◽  
2021 ◽  
Author(s):  
Janet S Duerr ◽  
John R McManus ◽  
John A Crowell ◽  
James B Rand
Keyword(s):  
Synaptic Vesicles ◽  
Neuromuscular Function ◽  
Temperature Sensitive ◽  
Temperature Dependent ◽  
Behavioral Deficits ◽  
Acetylcholine Synthesis ◽  
C Elegans ◽  
Protein Levels ◽  
Pumping Rates ◽  
Almost All

Abstract In Caenorhabditis elegans, the cha-1 gene encodes choline acetyltransferase (ChAT), the enzyme that synthesizes the neurotransmitter acetylcholine. We have analyzed a large number of cha-1 hypomorphic mutants, most of which are missense alleles. Some homozygous cha-1 mutants have approximately normal ChAT immunoreactivity; many other alleles lead to consistent reductions in synaptic immunostaining, although the residual protein appears to be stable. Regardless of protein levels, neuromuscular function of almost all mutants is temperature sensitive, i.e., neuromuscular function is worse at 25° than at 14°. We show that the temperature effects are not related to acetylcholine release, but specifically to alterations in acetylcholine synthesis. This is not a temperature-dependent developmental phenotype, because animals raised at 20° to young adulthood and then shifted for 2 hours to either 14° or 25° had swimming and pharyngeal pumping rates similar to animals grown and assayed at either 14° or 25°, respectively. We also show that the temperature-sensitive phenotypes are not limited to missense alleles; rather, they are a property of most or all severe cha-1 hypomorphs. We suggest that our data are consistent with a model of ChAT protein physically, but not covalently, associated with synaptic vesicles; and there is a temperature-dependent equilibrium between vesicle-associated and cytoplasmic (i.e., soluble) ChAT. Presumably, in severe cha-1 hypomorphs, increasing the temperature would promote dissociation of some of the mutant ChAT protein from synaptic vesicles, thus removing the site of acetylcholine synthesis (ChAT) from the site of vesicular acetylcholine transport. This, in turn, would decrease the rate and extent of vesicle-filling, thus increasing the severity of the behavioral deficits.

scholarly journals Inositol 1,4,5-Trisphosphate Signaling Regulates Mating Behavior in Caenorhabditis elegans Males

2005 ◽  
Vol 16 (9) ◽  
pp. 3978-3986 ◽  
Author(s):  
Nicholas J. D. Gower ◽  
Denise S. Walker ◽  
Howard A. Baylis
Keyword(s):  
Caenorhabditis Elegans ◽  
Male Fertility ◽  
Mating Disruption ◽  
Sperm Transfer ◽  
Male Mating ◽  
Turning Behavior ◽  
C Elegans ◽  
Inositol 1,4,5 Trisphosphate ◽  
Genes Encoding ◽  
Physiological Outcomes

Complex behavior requires the coordinated action of the nervous system and nonneuronal targets. Male mating in Caenorhabditis elegans consists of a series of defined behavioral steps that lead to the physiological outcomes required for successful impregnation. We demonstrate that signaling mediated by inositol 1,4,5-trisphosphate (IP3) is required at several points during mating. Disruption of IP3 receptor (itr-1) function results in dramatic loss of male fertility, due to defects in turning behavior (during vulva location), spicule insertion and sperm transfer. To elucidate the signaling pathways responsible, we knocked down the six C. elegans genes encoding phospholipase C (PLC) family members. egl-8, which encodes PLC-β, functions in spicule insertion and sperm transfer. itr-1 and egl-8 are widely expressed in the male reproductive system. An itr-1 gain-of-function mutation rescues infertility caused by egl-8 RNA interference, indicating that egl-8 and itr-1 function together as central components of the signaling events controlling sperm transfer.

scholarly journals Sub-cellular patterns of SPE-6 localization reveal unexpected complexities in C. elegans sperm activation and sperm function

2021 ◽  
Author(s):  
Jackson J Peterson ◽  
Claire E Tocheny ◽  
Gaurav Prajapati ◽  
Craig W LaMunyon ◽  
Diane C Shakes
Keyword(s):  
Plasma Membrane ◽  
Cellular Localization ◽  
Reproductive Tract ◽  
Female Reproductive Tract ◽  
Sperm Function ◽  
Temperature Sensitive ◽  
Casein Kinase 1 ◽  
Sperm Activation ◽  
C Elegans ◽  
Extracellular Signals

Abstract To acquire and maintain directed cell motility, Caenorhabditis elegans sperm must undergo extensive, regulated cellular remodeling, in the absence of new transcription or translation. To regulate sperm function, nematode sperm employ large numbers of protein kinases and phosphatases, including SPE-6, a member of C. elegans’ highly expanded casein kinase 1 superfamily. SPE-6 functions during multiple steps of spermatogenesis, including functioning as a “brake” to prevent premature sperm activation in the absence of normal extracellular signals. Here we describe the sub-cellular localization patterns of SPE-6 during wildtype C. elegans sperm development and in various sperm activation mutants. While other members of the sperm activation pathway associate with the plasma membrane or localize to the sperm’s membranous organelles, SPE-6 surrounds the chromatin mass of unactivated sperm. During sperm activation by either of two semiautonomous signaling pathways, SPE-6 redistributes to the front, central region of the sperm’s pseudopod. When disrupted by reduction-of-function alleles, SPE-6 protein is either diminished in a temperature-sensitive manner (hc187) or is mis-localized in a stage-specific manner (hc163). During the multistep process of sperm activation, SPE-6 is released from its perinuclear location after the spike stage in a process that does not require fusion of membranous organelles with the plasma membrane. After activation, spermatozoa exhibit variable proportions of perinuclear and pseudopod-localized SPE-6, depending on their location within the female reproductive tract. These findings provide new insights regarding SPE-6’s role in sperm activation and suggest that extracellular signals during sperm migration may further modulate SPE-6 localization and function.

scholarly journals Kindlin-2 in Sertoli cells is essential for testis development and male fertility in mice

2021 ◽  
Vol 12 (6) ◽  
Author(s):  
Xiaochun Chi ◽  
Weiwei Luo ◽  
Jiagui Song ◽  
Bing Li ◽  
Tiantian Su ◽  
...  
Keyword(s):  
Sertoli Cells ◽  
Male Fertility ◽  
Nuclear Translocation ◽  
Hippo Pathway ◽  
Reproductive Organs ◽  
Male Reproduction ◽  
Barrier Structure ◽  
Male Mice ◽  
Sperm Development

AbstractKindlin-2 is known to play important roles in the development of mesoderm-derived tissues including myocardium, smooth muscle, cartilage and blood vessels. However, nothing is known for the role of Kindlin-2 in mesoderm-derived reproductive organs. Here, we report that loss of Kindlin-2 in Sertoli cells caused severe testis hypoplasia, abnormal germ cell development and complete infertility in male mice. Functionally, loss of Kindlin-2 inhibits proliferation, increases apoptosis, impairs phagocytosis in Sertoli cells and destroyed the integration of blood-testis barrier structure in testes. Mechanistically, Kindlin-2 interacts with LATS1 and YAP, the key components of Hippo pathway. Kindlin-2 impedes LATS1 interaction with YAP, and depletion of Kindlin-2 enhances LATS1 interaction with YAP, increases YAP phosphorylation and decreases its nuclear translocation. For clinical relevance, lower Kindlin-2 expression and decreased nucleus localization of YAP was found in SCOS patients. Collectively, we demonstrated that Kindlin-2 in Sertoli cells is essential for sperm development and male reproduction.

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