scholarly journals The Caenorhabditis elegans proteasome subunit RPN ‐12 is required for hermaphrodite germline sex determination and oocyte quality

2020 ◽  
Author(s):  
Lourds M. Fernando ◽  
Jeandele Elliot ◽  
Anna K. Allen
Keyword(s):  
Caenorhabditis Elegans ◽  
Sex Determination ◽  
Oocyte Quality ◽  
Proteasome Subunit ◽  
Germline Sex Determination

scholarly journals The mog-1 gene is required for the switch from spermatogenesis to oogenesis in Caenorhabditis elegans.

Genetics ◽  
1993 ◽  
Vol 133 (4) ◽  
pp. 919-931 ◽  
Author(s):  
P L Graham ◽  
J Kimble
Keyword(s):  
Caenorhabditis Elegans ◽  
Sex Determination ◽  
Germ Cells ◽  
Germ Line ◽  
Loss Of Function ◽  
Wild Type ◽  
Per Se ◽  
Post Transcriptional Regulation ◽  
Germline Sex Determination ◽  
Embryonic Death

Abstract Caenorhabditis elegans hermaphrodites make first sperm, then oocytes. By contrast, animals homozygous for any of six loss-of-function mutations in the gene mog-1 (for masculinization of the germ line) make sperm continuously and do not switch into oogenesis. Therefore, in mog-1 mutants, germ cells that normally would become oocytes are transformed into sperm. By contrast, somatic sexual fates are normal, suggesting that mog-1 plays a germ line-specific role in sex determination. Analyses of double mutants suggest that mog-1 negatively regulates the fem genes and/or fog-1: mog-1; fem and mog-1; fog-1 double mutants all make oocytes rather than sperm. Therefore, we propose that wild-type mog-1 is required in the hermaphrodite germ line for regulation of the switch from spermatogenesis to oogenesis rather than for specification of oogenesis per se. In addition to its role in germline sex determination, maternal mog-1 is required for embryogenesis: most progeny of a mog-1; fem or mog-1; fog-1 mother die as embryos. How might the roles of mog-1 in the sperm/oocyte switch and embryogenesis be linked? Previous work showed that fem-3 is regulated post-transcriptionally to achieve the sperm/oocyte switch. We speculate that mog-1 may function in the post-transcriptional regulation of numerous germ-line RNAs, including fem-3. A loss of mog-1 might inappropriately activate fem-3 and thereby abolish the sperm/oocyte switch; its loss might also lead to misregulation of maternal RNAs and thus embryonic death.

scholarly journals Sperm fate is promoted by the mir-44 microRNA family in the Caenorhabditis elegans hermaphrodite germline

Genetics ◽  
2020 ◽  
Vol 217 (1) ◽  
Author(s):  
Katherine A Maniates ◽  
Benjamin S Olson ◽  
Allison L Abbott
Keyword(s):  
Gene Expression ◽  
Caenorhabditis Elegans ◽  
Sex Determination ◽  
Larval Development ◽  
Cell Fate ◽  
Rna Binding ◽  
Regulation Of Gene Expression ◽  
Cell Fate Decisions ◽  
Normal Period ◽  
Germline Sex Determination

Abstract Posttranscriptional regulation of gene expression, typically effected by RNA-binding proteins, microRNAs (miRNAs), and translation initiation factors, is essential for normal germ cell function. Numerous miRNAs have been detected in the germline; however, the functions of specific miRNAs remain largely unknown. Functions of miRNAs have been difficult to determine as miRNAs often modestly repress target mRNAs and are suggested to sculpt or fine tune gene expression to allow for the robust expression of cell fates. In Caenorhabditis elegans hermaphrodites, cell fate decisions are made for germline sex determination during larval development when sperm are generated in a short window before the switch to oocyte production. Here, analysis of newly generated mir-44 family mutants has identified a family of miRNAs that modulate the germline sex determination pathway in C. elegans. Mutants with the loss of mir-44 and mir-45 produce fewer sperm, showing both a delay in the specification and formation of sperm as well as an early termination of sperm specification accompanied by a premature switch to oocyte production. mir-44 and mir-45 are necessary for the normal period of fog-1 expression in larval development. Through genetic analysis, we find that mir-44 and mir-45 may act upstream of fbf-1 and fem-3 to promote sperm specification. Our research indicates that the mir-44 family promotes sperm cell fate specification during larval development and identifies an additional posttranscriptional regulator of the germline sex determination pathway.

scholarly journals The C. elegans proteasome subunit RPN-12 is required for hermaphrodite germline sex determination and oocyte quality

2020 ◽  
Author(s):  
Lourds M. Fernando ◽  
Jeandele Elliot ◽  
Anna K. Allen
Keyword(s):  
Sex Determination ◽  
Germ Line ◽  
Biological Significance ◽  
Oocyte Quality ◽  
26S Proteasome ◽  
Nuclear Accumulation ◽  
C Elegans ◽  
Chemical Inhibition ◽  
Higher Eukaryotes ◽  
Germline Sex Determination

AbstractBackgroundThe proteasome is a multi-subunit complex and a major proteolytic machinery in cells. Most subunits are essential for proteasome function, and depletion of individual subunits normally results in lethality. RPN-12/Rpn12/PSMD8 is a lid subunit of the 19S regulatory particle (RP) of the 26S proteasome. Studies in Caenorhabditis elegans demonstrated that RNAi depletion of RPN-12 does not result in lethality. RPN-12 has not been well studied in higher eukaryotes. In this study we investigate the biological significance of RPN-12 in C. elegans.ResultsWe found that the null mutant rpn-12(av93) did not cause major impairment of the proteolytic activity of the proteasome. Most rpn-12(av93) hermaphrodites lack sperm leading to feminization of the germ line that can be partially rescued by mating to males. The lack of sperm phenotype can be suppressed by downregulation of TRA-1, a player in the hermaphrodite germline sex determination pathway. Also, rpn-12(av93) animals show significant nuclear accumulation of the meiotic kinase WEE-1.3, a protein predominantly localized to the perinuclear region. Interestingly, chemical inhibition of the proteasome did not cause nuclear accumulation of WEE-1.3.ConclusionsRPN-12 plays a previously unknown role in oogenesis and the germline sex determination pathway in C. elegans hermaphrodites.

scholarly journals Nicotinamide Supplementation Improves Oocyte Quality and Offspring Development by Modulating Mitochondrial Function in an Aged Caenorhabditis elegans Model

Antioxidants ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 519
Author(s):  
Hyemin Min ◽  
Mijin Lee ◽  
Kyoung Sang Cho ◽  
Hyunjung Jade Lim ◽  
Yhong-Hee Shim
Keyword(s):  
Caenorhabditis Elegans ◽  
Mitochondrial Function ◽  
Stress Responses ◽  
Oocyte Quality ◽  
Embryonic Lethality ◽  
Reproductive Aging ◽  
Control Female ◽  
Offspring Development ◽  
Developmental Growth ◽  
Ros Accumulation

Aging is associated with a decline in the quality of biological functions. Among the aging processes, reproductive aging is a critical process because of its intergenerational effects. However, the mechanisms underlying reproductive aging remain largely unknown. Female reproductive aging is the primary reason for limited fertility in mammals. Therefore, we attempted to investigate a modulator that can control female reproductive aging using a Caenorhabditis elegans model. In the present study, we examined the role of nicotinamide (NAM) in oocyte quality and offspring development. The levels of reactive oxygen species (ROS) and oxidative stress responses in aged oocytes, embryonic lethality, and developmental growth of the offspring were examined with maternal NAM supplementation. Supplementation with NAM improved oocyte quality, decreased embryonic lethality, and promoted germ cell apoptosis. Furthermore, NAM supplementation in aged mothers reduced ROS accumulation and improved mitochondrial function in oocytes. Consequently, the developmental growth and motility of offspring were improved. These findings suggest that NAM supplementation improves the health of the offspring produced by aged mothers through improved mitochondrial function. Taken together, our results imply that NAM supplementation in the aged mother improves oocyte quality and protects offspring by modulating mitochondrial function.

Major sex-determining genes and the control of sexual dimorphism in Caenorhabditis elegans

Genome ◽  
1989 ◽  
Vol 31 (2) ◽  
pp. 625-637 ◽  
Author(s):  
Jonathan Hodgkin ◽  
Andrew D. Chisholm ◽  
Michael M. Shen
Keyword(s):  
Caenorhabditis Elegans ◽  
Sex Determination ◽  
X Chromosome ◽  
Germ Line ◽  
Cell Lineage ◽  
Regulatory Genes ◽  
Nematode Caenorhabditis Elegans ◽  
X Chromosomes ◽  
The Many ◽  
Lineage Analysis

Sex determination in Caenorhabditis elegans involves a cascade of major regulatory genes connecting the primary sex determining signal, X chromosome dosage, to key switch genes, which in turn direct development along either male or female pathways. Animals with one X chromosome (XO) are male, while animals with two X chromosomes (XX) are hermaphrodite: hermaphrodite development occurs because the action of the regulatory genes is modified in the germ line so that both sperm and oocytes are made inside a completely female soma. The regulatory genes are being examined by both genetic and molecular means. We discuss how these major genes, in particular the last switch gene in the cascade, tra-1, might regulate the many different sex-specific events that occur during the development of the hermaphrodite and of the male.Key words: nematode, Caenorhabditis elegans, sex determination, sexual differentiation, cell lineage analysis.

scholarly journals The role of Caenorhabditis elegans sex-determination homologs, Mi-sdc-1 and Mi-tra-1 in Meloidogyne incognita

2021 ◽  
Author(s):  
Anil Baniya ◽  
Soumi Joseph ◽  
Larry Duncan ◽  
William Crow ◽  
Tesfamariam Mengistu
Keyword(s):  
Caenorhabditis Elegans ◽  
Sex Determination ◽  
Meloidogyne Incognita ◽  
Egg Production ◽  
Target Genes ◽  
Parasitic Nematode ◽  
Plant Parasitic Nematode ◽  
Root Knot Nematode ◽  
Model Free ◽  
Plant Parasitic

AbstractSex determination is a key developmental event in all organisms. The pathway that regulates sexual fate has been well characterized at the molecular level in the model free-living nematode Caenorhabditis elegans. This study aims to gain a preliminary understanding of sex-determining pathways in a plant-parasitic nematode Meloidogyne incognita, and the extent to which the roles of the sex determination genes are conserved in a hermaphrodite species, C. elegans, and plant-parasitic nematode species, M. incognita. In this study, we targeted two sex-determining orthologues, sdc-1 and tra-1 from M. incognita using RNA interference (RNAi). RNAi was performed by soaking second-stage juveniles of M. incognita in a solution containing dsRNA of either Mi-tra-1or Mi-sdc-1 or both. To determine the effect of RNAi of the target genes, the juveniles treated with the dsRNA were inoculated onto a susceptible cultivar of cowpea grown in a nutrient pouch at 28 °C for 5 weeks. The development of the nematodes was analyzed at different time points during the growth period and compared to untreated controls. Our results showed that neither Mi-sdc-1 nor Mi-tra-1 have a significant role in regulating sexual fate in M. incognita. However, the silencing of Mi-sdc-1 significantly delayed maturity to adult females but did not affect egg production in mature females. In contrast, the downregulation of Mi-tra-1 transcript resulted in a significant reduction in egg production in both single and combinatorial RNAi-treated nematodes. Our results indicate that M. incognita may have adopted a divergent function for Mi-sdc-1 and Mi-tra-1distinct from Caenorhabditis spp. However, Mi-tra-1 might have an essential role in female fecundity in M. incognita and is a promising dsRNA target for root-knot nematode (RKN) management using host-delivered RNAi.

scholarly journals MORE SEX-DETERMINATION MUTANTS OF CAENORHABDITIS ELEGANS

Genetics ◽  
1980 ◽  
Vol 96 (3) ◽  
pp. 649-664 ◽  
Author(s):  
Jonathan Hodgkin
Keyword(s):  
Caenorhabditis Elegans ◽  
Sex Determination ◽  
X Chromosome ◽  
Constitutive Expression ◽  
Complementation Group ◽  
Sperm Production ◽  
Recessive Mutations ◽  
Her 2 ◽  
Map Location ◽  
Her Genes

ABSTRACT Sex determination in Caenorhabditis elegans is controlled by the X chromosome: autosome ratio, i.e. 2A;XX animals are hermaphrodite, and 2A;XO animals are male. A procedure for isolating 2A;XO animals that are transformed into hermaphrodites has been developed. Nine mutations causing this transformation have been obtained: eight are recessive, and all of these fall into a new autosomal complementation group, her-1 V. The remaining mutation (her-2) is dominant and has a genetic map location similar to that of tra-1 III. Recessive mutations of tra-1 cause the reverse transformation, transforming 2A;XX animals into males. Therefore, the her-2 mutation may result in constitutive expression of tra-1. Mutations in her-1 are without effect on XX animals, but the her-2 mutation prevents sperm production in both XX and XO animals, in addition to its effect on the sexual phenotype of XO animals. The epistatic relationships between tra and her genes are used to deduce a model for the action of these genes in controlling sex determination.

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