scholarly journals A dynamic DUO of regulatory proteins coordinates gamete specification and germ cell mitosis in the angiosperm male germline

2009 ◽  
Vol 4 (12) ◽  
pp. 1159-1162 ◽  
Author(s):  
Lynette Brownfield ◽  
David Twell
Keyword(s):  
Germ Cell ◽  
Regulatory Proteins ◽  
Male Germline ◽  
Gamete Specification ◽  
Cell Mitosis

scholarly journals Male germline development in the tammar wallaby, Macropus eugenii

Reproduction ◽  
2021 ◽  
Vol 161 (3) ◽  
pp. 333-341
Author(s):  
Teruhito Ishihara ◽  
Oliver W Griffith ◽  
Gerard A Tarulli ◽  
Marilyn B Renfree
Keyword(s):  
Dna Methylation ◽  
Germ Cell ◽  
Germ Cells ◽  
Evolutionary History ◽  
Tammar Wallaby ◽  
Mitotic Arrest ◽  
Germline Development ◽  
Macropus Eugenii ◽  
Male Germline ◽  
Cell Mitosis

Male germ cells undergo two consecutive processes – pre-spermatogenesis and spermatogenesis – to generate mature sperm. In eutherian mammals, epigenetic information such as DNA methylation is dynamically reprogrammed during pre-spermatogenesis, before and during mitotic arrest. In mice, by the time germ cells resume mitosis, the majority of DNA methylation is reprogrammed. The tammar wallaby has a similar pattern of germ cell global DNA methylation reprogramming to that of the mouse during early pre-spermatogenesis. However, early male germline development in the tammar or in any marsupial has not been described previously, so it is unknown whether this is a general feature regulating male germline development or a more recent phenomenon in mammalian evolutionary history. To answer this, we examined germ cell nuclear morphology and mitotic arrest during male germline development in the tammar wallaby (Macropus eugenii), a marsupial that diverged from mice and humans around 160 million years ago. Tammar pro-spermatogonia proliferated after birth and entered mitotic arrest after day 30 postpartum (pp). At this time, they began moving towards the periphery of the testis cords and their nuclear size increased. Germ cells increased in number after day 100 pp which is the time that DNA methylation is known to be re-established in the tammar. This is similar to the pattern observed in the mouse, suggesting that resumption of germ cell mitosis and the timing of DNA methylation reprogramming are correlated and conserved across mammals and over long evolutionary timescales.

scholarly journals Proliferation and cell fate establishment during Arabidopsis male gametogenesis depends on the Retinoblastoma protein

2009 ◽  
Vol 106 (17) ◽  
pp. 7257-7262 ◽  
Author(s):  
Zhong Chen ◽  
Said Hafidh ◽  
Shi Hui Poh ◽  
David Twell ◽  
Frederic Berger
Keyword(s):  
Cell Proliferation ◽  
Germ Cell ◽  
Cell Fate ◽  
Vegetative Cell ◽  
Germ Line ◽  
Sperm Cells ◽  
Cyclin Dependent Kinase ◽  
Rb Protein ◽  
Male Gametogenesis ◽  
Male Germline

The Retinoblastoma (Rb) protein is a conserved repressor of cell proliferation. In animals and plants, deregulation of Rb protein causes hyperproliferation and perturbs cell differentiation to various degrees. However, the primary developmental impact of the loss of Rb protein has remained unclear. In this study we investigated the direct consequences of Rb protein knockout in the Arabidopsis male germline using cytological and molecular markers. The Arabidopsis germ line derives from the unequal division of the microspore, producing a small germ cell and a large terminally differentiated vegetative cell. A single division of the germ cell produces the 2 sperm cells. We observed that the loss of Rb protein does not have a major impact on microspore division but causes limited hyperproliferation of the vegetative cell and, to a lesser degree, of the sperm cells. In addition, cell fate is perturbed in a fraction of Rb-defective vegetative cells. These defects are rescued by preventing cell proliferation arising from down-regulation of cyclin-dependent kinase A1. Our results indicate that hyperproliferation caused by the loss of Rb protein prevents or delays cell determination during plant male gametogenesis, providing further evidence for a direct link between fate determination and cell proliferation.

scholarly journals Regulation of BTB Dynamics in Spermatogenesis—Insights From the Adjudin Model

2019 ◽  
Vol 172 (1) ◽  
pp. 75-88 ◽  
Author(s):  
Bai-Ping Mao ◽  
Linxi Li ◽  
Ming Yan ◽  
Renshan Ge ◽  
Qingquan Lian ◽  
...  
Keyword(s):  
Germ Cell ◽  
Low Dose ◽  
Mammalian Target Of Rapamycin ◽  
Underlying Mechanism ◽  
Seminiferous Epithelium ◽  
Regulatory Proteins ◽  
Cell Organelles ◽  
Adult Rats ◽  
Downstream Signaling ◽  
Cellular Events

Abstract During spermatogenesis, cell organelles, and germ cells, most notably haploid spermatids, are transported across the seminiferous epithelium so that fully developed spermatids line-up at the edge of the tubule lumen to undergo spermiation at stage VIII of the cycle. Studies have suggested that the microtubule (MT)-based cytoskeleton is necessary to support these cellular events. However, the regulatory molecule(s) and underlying mechanism(s) remain poorly understood. Herein, we sought to better understand this event by using an adjudin-based animal model. Adult rats were treated with adjudin at low-dose (10 mg/kg b.w.) which by itself had no notable effects on spermatogenesis. Rats were also treated with low-dose adjudin combined with overexpression of 2 endogenously produced blood-testis barrier (BTB) modifiers, namely rpS6 (ribosomal protein S6, the downstream signaling protein of mammalian target of rapamycin complex 1 [mTORC1]) and F5-peptide (a biological active peptide released from laminin-γ3 chain at the Sertoli-spermatid interface) versus the 2 BTB modifiers alone. Overexpression of these 2 BTB modifiers in the testis was shown to enhance delivery of adjudin to the testis, effectively inducing disruptive changes in MT cytoskeletons, causing truncation of MT conferred tracks that led to their collapse across the epithelium. The net result was massive germ cell exfoliation in the tubules, disrupting germ cell transport and cell adhesion across the seminiferous epithelium that led to aspermatogenesis. These changes were the result of disruptive spatial expression of several MT-based regulatory proteins. In summary, MT cytoskeleton supported by the network of MT regulatory proteins is crucial to maintain spermatogenesis.

scholarly journals Wolbachia increase germ cell mitosis to enhance the fecundity of Laodelphax striatellus

2020 ◽  
Vol 127 ◽  
pp. 103471
Author(s):  
Yan Guo ◽  
Jehangir Khan ◽  
Xiao-Ying Zheng ◽  
Yu Wu
Keyword(s):  
Germ Cell ◽  
Laodelphax Striatellus ◽  
Cell Mitosis

The abnormal spindle protein is required for germ cell mitosis and oocyte differentiation during Drosophila oogenesis

2004 ◽  
Vol 298 (1) ◽  
pp. 96-106 ◽  
Author(s):  
Maria Giovanna Riparbelli ◽  
Chiara Massarelli ◽  
Leonard G Robbins ◽  
Giuliano Callaini
Keyword(s):  
Germ Cell ◽  
Drosophila Oogenesis ◽  
Oocyte Differentiation ◽  
Cell Mitosis

scholarly journals A long noncoding RNA binding to QKI-5 regulates germ cell apoptosis via p38 MAPK signaling pathway

2019 ◽  
Vol 10 (10) ◽  
Author(s):  
Kai Li ◽  
Shunshun Zhong ◽  
Yanyun Luo ◽  
Dingfeng Zou ◽  
Mengzhen Li ◽  
...  
Keyword(s):  
Germ Cell ◽  
Signaling Pathway ◽  
P38 Mapk ◽  
Cell Apoptosis ◽  
Rna Binding ◽  
Mapk Signaling ◽  
Mapk Signaling Pathway ◽  
Germline Development ◽  
Germ Cell Apoptosis ◽  
Male Germline

Abstract Spermatogenesis is the complex process of male germline development and requires coordinated interactions by multiple gene products that undergo strict developmental regulations. Increasing evidence has suggested that a number of long noncoding RNAs (lncRNAs) may function as important regulatory molecules in various physiological and pathological processes by binding to specific proteins. Here, we identified a subset of QKI-5-binding lncRNAs in the mouse testis through the integrated analyses of RNA immunoprecipitation (RIP)-microarray and biological verification. Among the lncRNAs, we revealed that NONMMUT074098.2 (Lnc10), which was highly expressed in the spermatogonia and spermatocytes of the testis, interacted with QKI-5. Furthermore, Lnc10 depletion promoted germ cell apoptosis via the activation of p38 MAPK, whereas the simultaneous knockdown of QKI-5 could rescue the apoptotic phenotype and the activation of p38 MAPK, which were induced by the loss of Lnc10. These data indicated that the Lnc10-QKI-5 interaction was associated with the regulatory roles of QKI-5 and that the Lnc10-QKI-5 interaction inhibited the regulation of QKI-5 on the downstream p38 MAPK signaling pathway. Additionally, we functionally characterized the biological roles of Lnc10 and found that the knockdown of Lnc10 promoted the apoptosis of spermatogenic cells in vivo; this suggested that Lnc10 had an important biological role in mouse spermatogenesis. Thus, our study provides a potential strategy to investigate the biological significance of lncRNA-RBP interactions during male germline development.

scholarly journals An autoregulatory switch in sex-specific phf7 transcription causes loss of sexual identity and tumors in the Drosophila female germline

2020 ◽  
Author(s):  
Anne E. Smolko ◽  
Laura Shapiro-Kulnane ◽  
Helen K. Salz
Keyword(s):  
Germ Cell ◽  
Sexual Identity ◽  
Germ Cells ◽  
Transcriptional Repression ◽  
Feedback Mechanism ◽  
Phd Finger ◽  
Transcriptional Reprogramming ◽  
Male Germline ◽  
Regulatory Circuit ◽  
Female Germline

ABSTRACTMaintenance of germ cell sexual identity is essential for reproduction. Entry into the spermatogenesis or oogenesis pathway requires that the appropriate gene network is activated and the antagonist network is silenced. For example, in Drosophila female germ cells, forced expression of the testis-specific PHD finger protein 7 (PHF7) disrupts oogenesis leading to either an agametic or germ cell tumor phenotype. Here we show that PHF7 expressing ovarian germ cells inappropriately express hundreds of genes, many of which are male germline genes. We find that the majority of genes under PHF7 control in female germ cells are not under PHF7 control in male germ cells, suggesting that PHF7 is acting in a tissue-specific manner. Remarkably, transcriptional reprogramming includes a positive autoregulatory feedback mechanism in which ectopic PHF7 overcomes its own transcriptional repression through promoter switching. Furthermore, we find that tumorigenic capacity is dependent on the dosage of phf7. This study reveals that high levels of ectopic PHF7 in female germ cells leads to a loss of sexual identity and promotion of a regulatory circuit beneficial for tumor initiation and progression.

scholarly journals tudor-domain containing protein 5-prime promotes male sexual identity in the Drosophila germline and is repressed in females by Sex lethal

2018 ◽  
Author(s):  
Shekerah Primus ◽  
Caitlin Pozmanter ◽  
Kelly Baxter ◽  
Mark Van Doren
Keyword(s):  
Germ Cell ◽  
Sexual Identity ◽  
Germ Cells ◽  
Expression Profiling ◽  
Female Identity ◽  
Rna Expression ◽  
Male Identity ◽  
Male Germline ◽  
Tudor Domain ◽  
Rna Expression Profiling

AbstractFor sexually reproducing organisms, production of male or female gametes depends on specifying the correct sexual identity in the germline. In D. melanogaster, Sex lethal (Sxl) is the key gene that controls sex determination in both the soma and the germline, but how it does so in the germline is unknown, other than that it is different than in the soma. We conducted an RNA expression profiling experiment to identify direct and indirect germline targets of Sxl specifically in the undifferentiated germline. We find that, in these cells, Sxl loss does not lead to a global masculinization observed at the whole-genome level. In contrast, Sxl appears to affect a discrete set of genes required in the male germline, such as Phf7. We also identify tudor domain containing protein 5-prime (tdrd5p) as a target for Sxl regulation that is important for male germline identity. tdrd5p is repressed by Sxl in female germ cells, but is highly expressed in male germ cells where it promotes proper male fertility and germline differentiation. Additionally, Tdrd5p localizes to cytoplasmic granules with some characteristics of RNA Processing (P-) Bodies, suggesting that it promotes male identity in the germline by regulating post-transcriptional gene expression.Author summaryLike humans, all sexually reproducing organisms require gametes to reproduce. Gametes are made by specialized cells called germ cells, which must have the correct sexual identity information to properly make sperm or eggs. In fruit flies, germ cell sexual identity is controlled by the RNA-binding protein Sxl, which is expressed only in females. To better understand how Sxl promotes female identity, we conducted an RNA expression profiling experiment to identify genes whose expression changes in response to the loss of Sxl from germ cells. Here, we identify tudor domain containing protein 5-prime (tdrd5p), which is expressed 17-fold higher in ovaries lacking Sxl compared to control ovaries. Additionally, tdrd5p plays an important role in males as male flies that are mutant for this gene cannot make sperm properly and thus are less fertile. Moreover, we find that tdrd5p promotes male identity in the germline, as several experiments show that it can shift the germ cell developmental program from female to male. This study tells us that Sxl promotes female identity in germ cells by repressing genes, like tdrd5p, that promote male identity. Future studies into the function of tdrd5p will provide mechanistic insight into how this gene promotes male identity.

scholarly journals A TWO-STAGE MODEL FOR THE CONTROL OF rDNA MAGNIFICATION

Genetics ◽  
1985 ◽  
Vol 109 (4) ◽  
pp. 691-700
Author(s):  
R Scott Hawley ◽  
Kenneth D Tartof
Keyword(s):  
Germ Cell ◽  
Stage Model ◽  
Two Stage ◽  
X Chromosomes ◽  
Germ Cell Development ◽  
Male Germline ◽  
Growth Properties ◽  
Large Clusters ◽  
Derivatives Of

ABSTRACT Males of the genotype bb/Ybb  - have been shown to produce both magnified (bbm  +) and, less frequently, reduced (bbrl) X chromosomes. An analysis of the progeny of single magnifying bb/Ybb- males reveals that bbm  + revertants may be recovered either as rare single events or, more frequently, in large clusters. To analyze the role of the bb phenotype in the induction of rDNA magnification we have constructed a series of bb and bb  + derivatives of Ybb-. Males carrying an X chromosomal bb allele and one of these derivatives (bb/bbYbb- or bb/bb  +  Ybb-) produce small numbers (one to two) of bbm  + progeny at a frequency similar to that observed for bb/Ybb- males but do not produce large clusters of bbm  + revertants. In addition, bb/bb  +  Ybb- males produce essentially equal numbers of magnified (bbm  +) and reduced (bbrl) X chromosomes. These data, together with a consideration of the growth properties of the male germline in Drosophila, suggest that magnification/reduction may occur at two different times during development. Those events that give rise to large clusters, and, thus, necessarily arise early in germ cell development, appear to be dependent on the bb phenotype. However, those events that give rise to single bbm  +chromosomes arise late in spermatogenesis, probably at meiosis, and are independent of the bb phenotype.

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