scholarly journals The Caenorhabditis elegans Homologue of Deleted in Azoospermia Is Involved in the Sperm/Oocyte Switch

2006 ◽  
Vol 17 (7) ◽  
pp. 3147-3155 ◽  
Author(s):  
Muneyoshi Otori ◽  
Takeshi Karashima ◽  
Masayuki Yamamoto

The Deleted in Azoospermia (DAZ) gene family encodes putative translational activators that are required for meiosis and other aspects of gametogenesis in animals. The single Caenorhabditis elegans homologue of DAZ, daz-1, is an essential factor for female meiosis. Here, we show that daz-1 is important for the switch from spermatogenesis to oogenesis (the sperm/oocyte switch), which is an essential step for the hermaphrodite germline to produce oocytes. RNA interference of the daz-1 orthologue in a related nematode, Caenorhabditis briggsae, resulted in a complete loss of the sperm/oocyte switch. The C. elegans hermaphrodite deficient in daz-1 also revealed a failure in the sperm/oocyte switch if the genetic background was conditional masculinization of germline. DAZ-1 could bind specifically to mRNAs encoding the FBF proteins, which are translational regulators for the sperm/oocyte switch and germ stem cell proliferation. Expression of the FBF proteins seemed to be lowered in the daz-1 mutant at the stage for the sperm/oocyte switch. Conversely, a mutation in gld-3, a gene that functionally counteracts FBF, could partially restore oogenesis in the daz-1 mutant. Together, we propose that daz-1 plays a role upstream of the pathway for germ cell sex determination.

1994 ◽  
Vol 14 (1) ◽  
pp. 484-491
Author(s):  
M MacMorris ◽  
J Spieth ◽  
C Madej ◽  
K Lea ◽  
T Blumenthal

The Caenorhabditis elegans vit genes, encoding vitellogenins, are abundantly expressed in the adult hermaphrodite intestine. Two repeated elements, vit promoter element 1 (VPE1 [TGTCAAT]) and VPE2 (CTGATAA), have been identified in the 5' flanking DNA of each of the vit genes of C. elegans and Caenorhabditis briggsae. These elements have previously been shown to be needed for correctly regulated expression of a vit-2/vit-6 fusion gene in low-copy-number, integrated transgenes. Here we extend the analysis of the function of VPE1 and VPE2 by using transgenic lines carrying large, extrachromosomal arrays of the test genes. The results validate the use of such arrays for transgenic analysis of gene regulation in C. elegans, by confirming previous findings showing that the VPE1 at -45 and both VPE2s are sites of activation. Additional experiments now indicate that when the -45 VPE1 is inverted or replaced by a VPE2, nearly total loss of promoter function results, suggesting that the highly conserved -45 VPE1 plays a unique role in vit-2 promoter function. In contrast, single mutations eliminating the three upstream VPE1s are without effect. However, in combination in double and triple mutants, these upstream VPE1 mutations cause drastic reductions in expression levels. The -150 VPE2 can be replaced by a XhoI site (CTCGAG), and the -90 VPE2 can be eliminated, as long as the overlapping VPE1 is left intact, but when these two replacements are combined, activity is lost. Thus, the promoter must have at least one VPE2 and it must have at least two VPE1s, one at -45 and one additional upstream element.


2021 ◽  
Vol 1 (1) ◽  
pp. 43-46
Author(s):  
A. V. Egorova ◽  
Т. В. Kalinnikova ◽  
R. R. Shagidullin

Heavy metals are one of the most common pollutants in environment. The aim of this work was to test the hypothesis assuming that one of mechanisms of toxic action of copper, cadmium and lead on invertebrates’ organisms is adaptive activation of cholinergic synaptic transmission. In experiments with two free-living soil nematodes, namely Caenorhabditis elegans and Caenorhabditis briggsae, it has been shown that Cu2+, Cd2+ and Pb2+ ions at concentrations of 60 and 120 µM enhanced the negative effects of the nicotinic acetylcholine receptors agonist levamisole on the nematodes’ organisms. Under combined action of levamisole and heavy metals on organisms of C. elegans and C. briggsae the mean time of nematodes paralysis (complete loss of the ability to swim) was reduced. The results of this work show that nematodes C. elegans and C. briggsae can be used as model organisms to study mechanisms of toxic action of heavy metals.


1994 ◽  
Vol 14 (1) ◽  
pp. 484-491 ◽  
Author(s):  
M MacMorris ◽  
J Spieth ◽  
C Madej ◽  
K Lea ◽  
T Blumenthal

The Caenorhabditis elegans vit genes, encoding vitellogenins, are abundantly expressed in the adult hermaphrodite intestine. Two repeated elements, vit promoter element 1 (VPE1 [TGTCAAT]) and VPE2 (CTGATAA), have been identified in the 5' flanking DNA of each of the vit genes of C. elegans and Caenorhabditis briggsae. These elements have previously been shown to be needed for correctly regulated expression of a vit-2/vit-6 fusion gene in low-copy-number, integrated transgenes. Here we extend the analysis of the function of VPE1 and VPE2 by using transgenic lines carrying large, extrachromosomal arrays of the test genes. The results validate the use of such arrays for transgenic analysis of gene regulation in C. elegans, by confirming previous findings showing that the VPE1 at -45 and both VPE2s are sites of activation. Additional experiments now indicate that when the -45 VPE1 is inverted or replaced by a VPE2, nearly total loss of promoter function results, suggesting that the highly conserved -45 VPE1 plays a unique role in vit-2 promoter function. In contrast, single mutations eliminating the three upstream VPE1s are without effect. However, in combination in double and triple mutants, these upstream VPE1 mutations cause drastic reductions in expression levels. The -150 VPE2 can be replaced by a XhoI site (CTCGAG), and the -90 VPE2 can be eliminated, as long as the overlapping VPE1 is left intact, but when these two replacements are combined, activity is lost. Thus, the promoter must have at least one VPE2 and it must have at least two VPE1s, one at -45 and one additional upstream element.


2013 ◽  
Vol 9 (1) ◽  
pp. 20120334 ◽  
Author(s):  
Chikako Matsuba ◽  
Dejerianne G. Ostrow ◽  
Matthew P. Salomon ◽  
Amit Tolani ◽  
Charles F. Baer

Mutation rate often increases with environmental temperature, but establishing causality is complicated. Asymmetry between physiological stress and deviation from the optimal temperature means that temperature and stress are often confounded. We allowed mutations to accumulate in two species of Caenorhabditis for approximately 100 generations at 18°C and for approximately 165 generations at 26°C; 26°C is stressful for Caenorhabditis elegans but not for Caenorhabditis briggsae . We report mutation rates at a set of microsatellite loci and estimates of the per-generation decay of fitness (Δ M w ), the genomic mutation rate for fitness ( U ) and the average effect of a new mutation ( E [ a ]), assayed at both temperatures. In C. elegans , the microsatellite mutation rate is significantly greater at 26°C than at 18°C whereas in C. briggsae there is only a slight, non-significant increase in mutation rate at 26°C, consistent with stress-dependent mutation in C. elegans . The fitness data from both species qualitatively reinforce the microsatellite results. The fitness results of C. elegans are potentially complicated by selection but also suggest temperature-dependent mutation; the difference between the two species suggests that physiological stress plays a significant role in the mutational process.


Genetics ◽  
1999 ◽  
Vol 152 (1) ◽  
pp. 221-235 ◽  
Author(s):  
Pascale Dufourcq ◽  
Philippe Chanal ◽  
Serge Vicaire ◽  
Elise Camut ◽  
Sophie Quintin ◽  
...  

Abstract lin-26, which encodes a unique Zn-finger protein, is required for differentiation of nonneuronal ectodermal cells in Caenorhabditis elegans. Here, we show that the two genes located immediately upstream of lin-26 encode LIN-26-like Zn-finger proteins; hence their names are lir-1 and lir-2 (lin-26 related). lir-2, lir-1, and lin-26 generate several isoforms by alternative splicing and/or trans-splicing at different positions. On the basis of their trans-splicing pattern, their intergenic distances, and their expression, we suggest that lir-2, lir-1, and lin-26 form two overlapping transcriptional operons. The first operon, which is expressed in virtually all cells, includes lir-2 and long lir-1 isoforms. The second operon, which is expressed in the nonneuronal ectoderm, includes short lir-1 isoforms, starting at exon 2 and lin-26. This unusual genomic organization has been conserved in C. briggsae, as shown by cloning the C. briggsae lir-2, lir-1, and lin-26 homologs. Particularly striking is the sequence conservation throughout the first lir-1 intron, which is very long in both species. Structural conservation is functionally meaningful as C. briggsae lin-26 is also expressed in the nonneuronal ectoderm and can complement a C. elegans lin-26 null mutation.


Development ◽  
2000 ◽  
Vol 127 (5) ◽  
pp. 1069-1079 ◽  
Author(s):  
T. Karashima ◽  
A. Sugimoto ◽  
M. Yamamoto

DAZ (Deleted in Azoospermia), the putative azoospermia factor gene in human, encodes a ribonucleoprotein-type RNA-binding protein required for spermatogenesis. A Drosophila homologue of DAZ, called boule, is also essential for spermatogenesis. A mouse homologue, Dazla, is implicated in both spermatogenesis and oogenesis. Here, we report the identification and characterization of daz-1, the single DAZ homologue in the nematode Caenorhabditis elegans. Loss of daz-1 function caused sterility in hermaphrodites, by blocking oogenesis at the pachytene stage of meiosis I. Epistasis analysis suggested that this gene executes its function succeeding gld-1, which governs the early pachytene stage in the oogenic pathway. Spermatogenesis did not appear to be affected in daz-1 hermaphrodites. Males defective in daz-1 produced sperm fully competent in fertilization. Analysis employing sex-determination mutants indicated that the daz-1 function was required for meiosis of female germline regardless of the sex of the soma. Transcription of daz-1 was restricted to the germline, starting prior to the onset of meiosis and was most conspicuous in cells undergoing oogenesis. Thus, daz-1 in C. elegans is an essential factor for female meiosis but, unlike other DAZ family members so far reported, it is dispensable for male meiosis.


eLife ◽  
2015 ◽  
Vol 4 ◽  
Author(s):  
Aitana Neves ◽  
Coralie Busso ◽  
Pierre Gönczy

All organisms live within a given thermal range, but little is known about the mechanisms setting the limits of this range. We uncovered cellular features exhibiting signature changes at thermal limits in Caenorhabditis elegans embryos. These included changes in embryo size and shape, which were also observed in Caenorhabditis briggsae, indicating evolutionary conservation. We hypothesized that such changes could reflect restricted aerobic capacity at thermal limits. Accordingly, we uncovered that relative respiration in C. elegans embryos decreases at the thermal limits as compared to within the thermal range. Furthermore, by compromising components of the respiratory chain, we demonstrated that the reliance on aerobic metabolism is reduced at thermal limits. Moreover, embryos thus compromised exhibited signature changes in size and shape already within the thermal range. We conclude that restricted aerobic metabolism at the thermal limits contributes to setting the thermal range in a metazoan organism.


2002 ◽  
Vol 69 ◽  
pp. 117-134 ◽  
Author(s):  
Stuart M. Haslam ◽  
David Gems ◽  
Howard R. Morris ◽  
Anne Dell

There is no doubt that the immense amount of information that is being generated by the initial sequencing and secondary interrogation of various genomes will change the face of glycobiological research. However, a major area of concern is that detailed structural knowledge of the ultimate products of genes that are identified as being involved in glycoconjugate biosynthesis is still limited. This is illustrated clearly by the nematode worm Caenorhabditis elegans, which was the first multicellular organism to have its entire genome sequenced. To date, only limited structural data on the glycosylated molecules of this organism have been reported. Our laboratory is addressing this problem by performing detailed MS structural characterization of the N-linked glycans of C. elegans; high-mannose structures dominate, with only minor amounts of complex-type structures. Novel, highly fucosylated truncated structures are also present which are difucosylated on the proximal N-acetylglucosamine of the chitobiose core as well as containing unusual Fucα1–2Gal1–2Man as peripheral structures. The implications of these results in terms of the identification of ligands for genomically predicted lectins and potential glycosyltransferases are discussed in this chapter. Current knowledge on the glycomes of other model organisms such as Dictyostelium discoideum, Saccharomyces cerevisiae and Drosophila melanogaster is also discussed briefly.


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