A New Dataset of Spermatogenic <i>vs.</i> Oogenic Transcriptomes in the Nematode <i>Caenorhabditis elegans</i>

Ortiz, Marco Antonio; Noble, Daniel; Sorokin, Elena P.; Kimble, Judith

doi:10.1534/g3.114.012351

Cited by 154 publications

(299 citation statements)

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“…We compared csr-1(RNAi) upregulated genes with available gamete-enriched datasets (Chu et al, 2006;Ortiz et al, 2014;Reinke et al, 2004). As with P-granule RNAi, we found that oocyte-enriched genes are slightly downregulated, whereas sperm-enriched genes are highly upregulated following csr-1 RNAi (Fig.…”

Section: Expression In Csr-1-depleted Germlinesmentioning

confidence: 94%

“…P granules function to repress sperm-specific mRNA accumulation in the hermaphrodite germline Gene ontology analysis of upregulated set 1 genes following P-granule RNAi shows an enrichment in terms associated with spermatogenesis. We therefore compared upregulated set 1 genes with available gamete-enriched datasets (Chu et al, 2006;Ortiz et al, 2014;Reinke et al, 2004). We found that oocyte-enriched genes are slightly downregulated, whereas sperm-enriched genes are highly upregulated following P-granule RNAi (Fig.…”

Section: Expression In P-granule-depleted Germlinesmentioning

confidence: 99%

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CSR-1 and P granules suppress sperm-specific transcription in theC. elegansgermline

Campbell

Updike

2015

Development

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Germ granules (P granules) in C. elegans are required for fertility and function to maintain germ cell identity and pluripotency. Sterility in the absence of P granules is often accompanied by the misexpression of soma-specific proteins and the initiation of somatic differentiation in germ cells. To investigate whether this is caused by the accumulation of somatic transcripts, we performed mRNA-seq on dissected germlines with and without P granules. Strikingly, we found that somatic transcripts do not increase in the young adult germline when P granules are impaired. Instead, we found that impairing P granules causes sperm-specific mRNAs to become highly overexpressed. This includes the accumulation of major sperm protein (MSP) transcripts in germ cells, a phenotype that is suppressed by feminization of the germline. A core component of P granules, the endo-siRNA-binding Argonaute protein CSR-1, has recently been ascribed with the ability to license transcripts for germline expression. However, impairing CSR-1 has very little effect on the accumulation of its mRNA targets. Instead, we found that CSR-1 functions with P granules to prevent MSP and sperm-specific mRNAs from being transcribed in the hermaphrodite germline. These findings suggest that P granules protect germline integrity through two different mechanisms, by (1) preventing the inappropriate expression of somatic proteins at the level of translational regulation, and by (2) functioning with CSR-1 to limit the domain of sperm-specific expression at the level of transcription.

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Section: Expression In Csr-1-depleted Germlinesmentioning

confidence: 94%

Section: Expression In P-granule-depleted Germlinesmentioning

confidence: 99%

CSR-1 and P granules suppress sperm-specific transcription in theC. elegansgermline

Campbell

Updike

2015

Development

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“…By contrast, the 84 mRNAs reduced in puf-8; lip-1 vs. puf-8 fbf-1; lip-1 were not enriched for oogenic mRNAs from either list (Figure 3, C and D). Finally, we compared our lists of increased and decreased mRNAs with a recent data set of mRNAs enriched in dissected oogenic gonads (Ortiz et al 2014) and found a similar significant enrichment for the increased mRNAs (53%, 72/134; hypergeometric distribution, FDR , 1E-24), but not for the decreased mRNAs. We conclude that puf-8; lip-1 animals express high levels of oogenic mRNAs relative to puf-8 fbf-1; lip-1 animals.…”

Section: Sperm-only Adults Differ In Reprogramming Competencementioning

confidence: 77%

“…According to NEXTDB the 335 mRNAs were significantly enriched for oogenic transcripts ( Figure 4C), maternal mRNAs ( Figure 4D), oogenic mRNAs ( Figure 4E), EFL-1 targets ( Figure 4F) and GLD-1 mRNA targets ( Figure 4G) (FDR # 1E-6). Additionally, of these 335 mRNAs, 255 were also enriched in oogenic gonads compared to spermatogenic gonads (Ortiz et al 2014) (FDR ,. We conclude that the fbf-1; lip-1 transcriptome, like the puf-8; lip-1 transcriptome, is enriched for mRNAs linked to oogenesis, even though both mutants make only sperm.…”

Section: Sperm-only Adults Differ In Reprogramming Competencementioning

confidence: 99%

Competence for Chemical Reprogramming of Sexual Fate Correlates with an Intersexual Molecular Signature inCaenorhabditis elegans

2014

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In multicellular organisms, genetic programs guide cells to adopt cell fates as tissues are formed during development, maintained in adults, and repaired after injury. Here we explore how a small molecule in the environment can switch a genetic program from one fate to another. Wild-type Caenorhabditis elegans XX adult hermaphrodites make oocytes continuously, but certain mutant XX adults make sperm instead in an otherwise hermaphrodite soma. Thus, puf-8; lip-1 XX adults make only sperm, but they can be switched from sperm to oocyte production by treatment with a small-molecule MEK inhibitor. To ask whether this chemical reprogramming is common, we tested six XX sperm-only mutants, but found only one other capable of cell fate switching, fbf-1; lip-1. Therefore, reprogramming competence relies on genotype, with only certain mutants capable of responding to the MEK inhibitor with a cell fate change. To gain insight into the molecular basis of competence for chemical reprogramming, we compared polyadenylated transcriptomes of competent and noncompetent XX sperm-only mutants in the absence of the MEK inhibitor and hence in the absence of cell fate reprogramming. Despite their cellular production of sperm, competent mutants were enriched for oogenic messenger RNAs relative to mutants lacking competence for chemical reprogramming. In addition, competent mutants expressed the oocyte-specific protein RME-2, whereas those lacking competence did not. Therefore, mutants competent for reprogramming possess an intersexual molecular profile at both RNA and protein levels. We suggest that this intersexual molecular signature is diagnostic of an intermediate network state that poises the germline tissue for changing its cellular fate in response to environmental cues. C ELLS in multicellular organisms acquire specific fates, either during development as tissues are generated or during adulthood as tissues are renewed or repaired. A classical view holds that during development, a cell follows a specific genetic program to determine its differentiated fate, but more recent studies reveal that cells can be induced to switch from one genetic program to another. Such "reprogramming" of a cell fate program can occur in vivo in cancer (Friedl and Alexander 2011;Byun and Gardner 2013), wound healing (Wong et al. 2013), and regeneration (Xin et al. 2013;Ziv et al. 2013). Moreover, reprogramming can be stimulated by introduction of transcription factors (Takahashi and Yamanaka 2006) or small molecules (Morgan et al. 2010;Zhu et al. 2010;Li et al. 2014). Here we explore the effect of genotype on the capacity for a particular case of chemically induced cell fate reprogramming within an organism.The Caenorhabditis elegans germline provides a tractable model for analyses of cell fate reprogramming. The adult germline is an elongate tissue with 2000 cells, including germline stem cells (GSCs) (Figure 1A, yellow). GSCs continuously generate daughter cells that enter the meiotic cell cycle ( Figure 1A, green) and then differentiate as...

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“…To test if X chromosome number contributes to hermaphrodite-biased expression specifically in the germline, we used germline and soma expression categories defined in a recent study that measured gene expression in dissected hermaphrodite oogenic gonads (Ortiz et al 2014). We grouped genes with no, low, and high germline expression using cutoffs FPKM , 1, 1 , FPKM , 10, and FPKM .…”

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confidence: 99%

Untangling the Contributions of Sex-Specific Gene Regulation and X-Chromosome Dosage to Sex-Biased Gene Expression in Caenorhabditis elegans

Kramer¹,

Rao²,

Ercan

2016

Genetics

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Dosage compensation mechanisms equalize the level of X chromosome expression between sexes. Yet the X chromosome is often enriched for genes exhibiting sex-biased, i.e., imbalanced expression. The relationship between X chromosome dosage compensation and sex-biased gene expression remains largely unexplored. Most studies determine sex-biased gene expression without distinguishing between contributions from X chromosome copy number (dose) and the animal's sex. Here, we uncoupled X chromosome dose from sex-specific gene regulation in Caenorhabditis elegans to determine the effect of each on X expression. In early embryogenesis, when dosage compensation is not yet fully active, X chromosome dose drives the hermaphrodite-biased expression of many X-linked genes, including several genes that were shown to be responsible for hermaphrodite fate. A similar effect is seen in the C. elegans germline, where X chromosome dose contributes to higher hermaphrodite X expression, suggesting that lack of dosage compensation in the germline may have a role in supporting higher expression of X chromosomal genes with female-biased functions in the gonad. In the soma, dosage compensation effectively balances X expression between the sexes. As a result, somatic sex-biased expression is almost entirely due to sex-specific gene regulation. These results suggest that lack of dosage compensation in different tissues and developmental stages allow X chromosome copy number to contribute to sex-biased gene expression and function.KEYWORDS dosage compensation; C. elegans; RNA-seq; sex; sex-biased gene expression; chromatin; X chromosome; transcription; gene regulation; germline; XO; genetics of sex M ALES and females exhibit many phenotypic differences, termed sexual dimorphisms. With the exception of the gene-poor Y chromosome, the two sexes share identical genomes. Thus, sexual dimorphisms stem from differences in gene expression between sexes. Genes that are expressed differently between sexes include those expressed exclusively (sex specific) or at a higher level in one sex (sex biased). Sexbiased expression allows a gene to be more active in the sex that it benefits without a potential cost to the opposite sex. Sex-biased gene expression is common throughout metazoans. Previous studies indicate up to 60% of all genes show sex-biased expression [in mice (Khil et al. 2004;Yang et al. 2006;Reinius et al. 2012), flies (Parisi et al. 2003;Ranz et al. 2003;Allen et al. 2013;Kaiser and Bachtrog 2014), and nematodes (Reinke et al. 2004;Thomas et al. 2012;Albritton et al. 2014)].Previous genome-wide studies found that compared to autosomes, the X chromosome generally harbors more genes with female-biased expression and fewer genes with malebiased expression [in mice (Khil et al. 2004;Yang et al. 2006;Reinius et al. 2012), flies (Parisi et al. 2003;Ranz et al. 2003), and nematodes (Reinke et al. 2004;Thomas et al. 2012;Albritton et al. 2014)]. However, this observed enrichment of female bias and depletion of male bias from the X is a gene...

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A New Dataset of Spermatogenic vs. Oogenic Transcriptomes in the Nematode Caenorhabditis elegans

Cited by 154 publications

References 42 publications

CSR-1 and P granules suppress sperm-specific transcription in theC. elegansgermline

CSR-1 and P granules suppress sperm-specific transcription in theC. elegansgermline

Competence for Chemical Reprogramming of Sexual Fate Correlates with an Intersexual Molecular Signature inCaenorhabditis elegans

Untangling the Contributions of Sex-Specific Gene Regulation and X-Chromosome Dosage to Sex-Biased Gene Expression in Caenorhabditis elegans

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