144. MAELSTROM - A PROTEIN THAT IS ESSENTIAL FOR SPERMATOGENESIS AND TRANSPOSABLE REPRESSION IS EXPRESSED IN ADULT OVARY OF MAMMALS AND BIRDS

2010 ◽  
Vol 22 (9) ◽  
pp. 62
Author(s):  
S. Lim ◽  
E. Tsend-Ayush ◽  
R. Kortschak ◽  
C. Ricciardelli ◽  
M. Oehler ◽  
...  

Maelstrom (MAEL) is a highly evolutionarily conserved protein located at the perinuclear structure of animal germ cells called nuage. The MAEL protein contains HMG and Tudor domains and associates with components of the piRNA and RNAi pathways and chromatin remodelling factors. Recent work has shown that MAEL is required for the differentiation of the germ-line stem cell lineage and for the retroposon repression. In mouse, Mael is expressed in male germ cells and is essential for spermatogenesis and retroposon suppression. We have investigated the evolution of the Mael gene in mammals and birds. As expected the gene is highly conserved in all three mammalian lineages and in chicken. Interestingly, the platypus MAEL has exclusive changes in the DnaQ-H 3’-5’ exonuclease domain and computational modelling suggested that these changes may affect the folding of the protein. Expression analysis revealed that the Mael gene is transcribed in testis but also in adult ovaries of chicken, platypus, mouse and human. In situ hybridisation of the Mael transcript on ovary sections of mouse and platypus shows that gene expression is found in pre-antral and antral follicles. The data so far also showed some differences in the expression pattern between mouse and platypus. In mouse, we detected transcript in oocyte, granulosa cells and cumulus cells whereas in the platypus we only observed expression in oocyte. Earlier work demonstrated that Drosophila Mael mutant ovaries had mislocalisation of the RNAi pathway proteins, Dicer and Argonaute2. It is well known that RNAi pathyway is involved in the repression of transposon in the testis and ovary across animal kingdom. As a key component of the RNAi pathway, MAEL is reported to co-localise and interact with MILI and MIWI proteins. These finding may suggest a role of MAEL in retroposon control in ovary and folliculogenesis.

Genetics ◽  
2004 ◽  
Vol 167 (2) ◽  
pp. 707-723 ◽  
Author(s):  
Cordula Schulz ◽  
Amy A. Kiger ◽  
Salli I. Tazuke ◽  
Yukiko M. Yamashita ◽  
Luiz C. Pantalena-Filho ◽  
...  

Development ◽  
2022 ◽  
Author(s):  
Yuki Naitou ◽  
Go Nagamatsu ◽  
Nobuhiko Hamazaki ◽  
Kenjiro Shirane ◽  
Masafumi Hayashi ◽  
...  

In mammals, primordial germ cells (PGCs), the origin of the germ line, are specified from the epiblast at the posterior region where gastrulation simultaneously occurs, yet the functional relationship between PGC specification and gastrulation remains unclear. Here, we show that Ovol2, a transcription factor conserved across the animal kingdom, balances these major developmental processes by repressing the epithelial-to-mesenchymal transition (EMT) driving gastrulation and the upregulation of genes associated with PGC specification. Ovol2a, a splice variant encoding a repressor domain, directly regulates EMT-related genes and consequently induces re-acquisition of potential pluripotency during PGC specification, whereas Ovol2b, another splice variant missing the repressor domain, directly upregulates genes associated with PGC specification. Taken together, these results elucidate the molecular mechanism underlying allocation of the germ line among epiblast cells differentiating into somatic cells through gastrulation.


eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Alexis S Bailey ◽  
Pedro J Batista ◽  
Rebecca S Gold ◽  
Y Grace Chen ◽  
Dirk G de Rooij ◽  
...  

The switch from mitosis to meiosis is the key event marking onset of differentiation in the germline stem cell lineage. In Drosophila, the translational repressor Bgcn is required for spermatogonia to stop mitosis and transition to meiotic prophase and the spermatocyte state. Here we show that the mammalian Bgcn homolog YTHDC2 facilitates a clean switch from mitosis to meiosis in mouse germ cells, revealing a conserved role for YTHDC2 in this critical cell fate transition. YTHDC2-deficient male germ cells enter meiosis but have a mixed identity, maintaining expression of Cyclin A2 and failing to properly express many meiotic markers. Instead of continuing through meiotic prophase, the cells attempt an abnormal mitotic-like division and die. YTHDC2 binds multiple transcripts including Ccna2 and other mitotic transcripts, binds specific piRNA precursors, and interacts with RNA granule components, suggesting that proper progression of germ cells through meiosis is licensed by YTHDC2 through post-transcriptional regulation.


2018 ◽  
Author(s):  
Fani Papagiannouli ◽  
Cameron Wynn Berry ◽  
Margaret T. Fuller

SUMMARYTissue homeostasis and repair relies on proper communication of stem cells and their differentiating daughters with the local tissue microenvironment. In the Drosophila male germline adult stem cell lineage, germ cells proliferate and progressively differentiate enclosed in supportive somatic cyst cells, forming a small organoid, the functional unit of differentiation. Here we show that cell polarity and vesicle trafficking influence signal transduction in cyst cells, with profound effects on the germ cells they enclose. Our data suggest that both the cortical components Dlg, Scrib, Lgl and the clathrin-mediated endocytic (CME) machinery downregulate EGFR signaling. Knockdown of dlg, scrib, lgl or CME components in cyst cells resulted in germ cell death, similar to increased signal transduction via the EGFR, while lowering EGFR or downstream signaling components rescued the defects. This work provides new insights on how cell polarity and endocytosis cooperate to regulate signal transduction and sculpt developing tissues.


2009 ◽  
Vol 21 (9) ◽  
pp. 2
Author(s):  
P. Western ◽  
J. Van Den Bergen ◽  
D. Miles ◽  
R. Ralli ◽  
A. Sinclair

The germ cell lineage is unique in that it must ensure that the genome retains the complete developmental potential (totipotency) that supports development in the following generation. This is achieved through a number of mechanisms that prevent the early germ cell lineage from somatic differentiation and promote the capactity for functional totipotency. Part of this process involves the retained germ line expression of key genes that regulate pluripotency in embryonic stem cells, embryonic germ cells and some embryonal carcinoma cells, the stem cells of testicular tumours. Despite this, germ cells are not intrinsically pluripotent and must differentiate along the male or female pathways, a process which requires commitment of the bi-potential primordial germ cells to the spermatogenic (male) pathway and their entry into mitotic arrest, or to the oogenic pathway (females) and entry into meiosis. This involves robust regulation of regulatory networks controlling pluripotency, cell cycle and sex specific differentiation. Our work aims to further understand the mechanisms controlling differentiation, pluripotency and cell cycle in early male and female germ cells. Our data shows that mitotic arrest of male germ cells involves strict regulation of the G1-S phase check-point through the retinoblastoma protein. In addition, suppression of pluripotency in differentiating male germ cells involves post-transcriptional regulation of OCT4, transcriptional regulation of Sox2 and Nanog and methylation of the Sox2 and Nanog promoters. Further understanding of these processes promises to lead to a greater understanding of the molecular mechanisms underlying control of pluripotency, cell cycle and differentiation in the germ line and the initiation of germ cell derived testis tumours.


Development ◽  
1997 ◽  
Vol 124 (21) ◽  
pp. 4361-4371 ◽  
Author(s):  
P. Gonczy ◽  
E. Matunis ◽  
S. DiNardo

Stem cells divide asymmetrically, regenerating a parental stem cell and giving rise to a daughter cell with a distinct fate. In many stem cell lineages, this daughter cell undergoes several amplificatory mitoses, thus generating more cells that embark on the differentiation program specific for the given lineage. Spermatogenesis in Drosophila is a model system to identify molecules regulating stem cell lineages. Mutations at two previously identified loci, bag-of-marbles (bam) and benign gonial cell neoplasm (bgcn), prevent progression through spermatogenesis and oogenesis, resulting in the overproliferation of undifferentiated germ cells. Here we investigate how bam and bgcn regulate the male germline stem cell lineage. By generating FLP-mediated clones, we demonstrate that both bam and bgcn act autonomously in the germline to restrict proliferation during spermatogenesis. By using enhancer trap lines, we find that the overproliferating germ cells express markers specific to amplifying germ cells, while at the same time retaining the expression of some markers of stem cell and primary spermatogonial cell fate. However, we find that germ cells accumulating in bam or bgcn mutant testes most resemble amplifying germ cells, because they undergo incomplete cytokinesis and progress through the cell cycle in synchrony within a cyst, which are two characteristics of amplifying germ cells, but not of stem cells. Taken together, our results suggest that bam and bgcn regulate progression through the male germline stem cell lineage by cell-intrinsically restricting the proliferation of amplifying germ cells.


2011 ◽  
Vol 2011 ◽  
pp. 1-15 ◽  
Author(s):  
Massimo De Felici

The unique capability of germ cells to give rise to a new organism, allowing the transmission of primary genetic information from generation to generation, depends on their epigenetic reprogramming ability and underlying genomic totipotency. Recent studies have shown that genome-wide epigenetic modifications, referred to as “epigenetic reprogramming”, occur during the development of the gamete precursors termed primordial germ cells (PGCs) in the embryo. This reprogramming is likely to be critical for the germ line development itself and necessary to erase the parental imprinting and setting the base for totipotency intrinsic to this cell lineage. The status of genome acquired during reprogramming and the associated expression of key pluripotency genes render PGCs susceptible to transform into pluripotent stem cells. This may occurin vivounder still undefined condition, and it is likely at the origin of the formation of germ cell tumors. The phenomenon appears to be reproduced under partly definedin vitroculture conditions, when PGCs are transformed into embryonic germ (EG) cells. In the present paper, I will try to summarize the contribution that epigenetic modifications give to nuclear reprogramming in mouse PGCs.


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