scholarly journals Discrete somatic niches coordinate proliferation and migration of primordial germ cells via Wnt signaling

2016 ◽  
Vol 214 (2) ◽  
pp. 215-229 ◽  
Author(s):  
Andrea V. Cantú ◽  
Svetlana Altshuler-Keylin ◽  
Diana J. Laird
Keyword(s):  
Cell Cycle ◽  
Germ Cell ◽  
Wnt Signaling ◽  
Germ Cells ◽  
Primordial Germ Cells ◽  
Early Embryo ◽  
Cell Pool ◽  
And Migration ◽  
Selective Mechanism ◽  
Proliferation And Migration

Inheritance depends on the expansion of a small number of primordial germ cells (PGCs) in the early embryo. Proliferation of mammalian PGCs is concurrent with their movement through changing microenvironments; however, mechanisms coordinating these conflicting processes remain unclear. Here, we find that PGC proliferation varies by location rather than embryonic age. Ror2 and Wnt5a mutants with mislocalized PGCs corroborate the microenvironmental regulation of the cell cycle, except in the hindgut, where Wnt5a is highly expressed. Molecular and genetic evidence suggests that Wnt5a acts via Ror2 to suppress β-catenin–dependent Wnt signaling in PGCs and limit their proliferation in specific locations, which we validate by overactivating β-catenin in PGCs. Our results suggest that the balance between expansion and movement of migratory PGCs is fine-tuned in different niches by the opposing β-catenin–dependent and Ror2-mediated pathways through Wnt5a. This could serve as a selective mechanism to favor early and efficient migrators with clonal dominance in the ensuing germ cell pool while penalizing stragglers.

Memoirs: Studies on the Germ-cell Cycle of Cryptocotyle lingua

1934 ◽  
Vol s2-76 (304) ◽  
pp. 573-614
Author(s):  
RAYMOND MILLARD CABLE
Keyword(s):  
Cell Cycle ◽  
Germ Cell ◽  
Germ Cells ◽  
Alternative Hypothesis ◽  
Primordial Germ Cells ◽  
Body Cavity ◽  
The Body ◽  
Larval Stages ◽  
Nuclear Changes ◽  
New Hosts

The writer's earlier study (Cable, 1931) on the germ-cell cycle in the adult stage of Cryptocotyle lingua is supplemented by an investigation of germinal development in the larval stages occurring in the marine snail, Littorina littorea. The miracidium-mother-sporocyst was not found although very young rediae were abundant in the material studied. The primordial germ-cells of the young redia are observed in an undifferentiated condition in the body-cavity, which is not well defined due to an abundance of connective tissue. After a period of differentiation, including growth, progressive nuclear changes, and condensation of cytoplasm, the germ-cells multiply by equal division, a process which is interpreted as polyembryony. Germinal differentiation exhibits a distinct anterior-posterior gradient. The mature germinal cells give rise directly to cercarial embryos without germ-mass formation and dissociation or any maturation processes. Although germinal lineage may be traced in the redia, it seems to be interrupted in the cercaria, due to delayed segregation of germ-cells. The soma of the redia does not produce germ-cells at any stage. Evidence is afforded by this and other studies that germinal lineage with sudden intercalations of polyembryonic stages (germ-masses) cannot explain the germinal cycle of the trematodes as a group. In an alternative hypothesis, based on the phylogeny of the Digenea, it is suggested that the ancestors of this group became sexually mature in the mollusc and completed the cycle in that host, possibly before the appearance of vertebrates; and that, with the evolution of the trematodes, sexual phenomena have gradually been lost, while accessory stages and new hosts have been included in the life-cycle. Cryptocotyle lingua is assumed to have been modified to an intermediate extent since sexual reproduction, germ-masses, and the maximum number of intercalary stages are lacking in the larval generations.

Biology of human testicular germ cell tumours

1999 ◽  
Vol 7 (2) ◽  
pp. 141-154
Author(s):  
Martin F Pera
Keyword(s):  
Stem Cells ◽  
Germ Cell ◽  
Germ Cells ◽  
Primordial Germ Cells ◽  
Germ Cell Tumour ◽  
Early Embryo ◽  
Germ Cell Tumours ◽  
Testicular Germ Cell ◽  
Testicular Germ Cell Tumours ◽  
Wide Range

Testicular germ cell tumours are a rare and bizarre diversion in the life cycle of the male germ line. These neoplasms are thought to originate during embryonic life from primordial germ cells (PGCs) which fail to undergo maturation into prospermatogonia. Maturation arrest and the development of aneuploidy in the PGC give rise to the precursor of germ cell malignancy, the testicular carcinoma in situ (CIS) cell. Thereafter, a complex series of genetic changes, coupled with the onset of puberty, can either convert the CIS cell into a malignant tumour made up of cells resembling primordial germ cells (a seminoma), or drive it down a pathway akin to parthenogenesis, so that it acquires a special property shared with cells of the early embryo – pluripotentiality, or the ability to differentiate into a wide range of somatic cells. The latter form of germ cell tumour, a teratocarcinoma, will contain primitive undifferentiated stem cells and multiple somatic tissues representing derivatives of all three germ layers plus the extraembryonic membranes which support development. Pluripotentiality is a property common to the oocyte, the cells of the early embryo up to the stage just after implantation, primordial germ cells, and the stem cells of germ cell tumours (Figure 1).

Primordial germ cell migration in Drosophila melanogaster is controlled by somatic tissue

Development ◽  
1994 ◽  
Vol 120 (1) ◽  
pp. 83-89 ◽  
Author(s):  
M.K. Jaglarz ◽  
K.R. Howard
Keyword(s):  
Germ Cell ◽  
Germ Cells ◽  
Characteristic Time ◽  
Primordial Germ Cells ◽  
Primordial Germ Cell ◽  
Somatic Tissue ◽  
Migratory Behavior ◽  
Somatic Tissues ◽  
Germ Cell Migration ◽  
And Migration

In Drosophila, as in many other organisms, primordial germ cells show invasive and migratory behavior moving from their site of origin to the somatic component of the gonad. At a characteristic time in development, the primordial germ cells pass across the primordium of the gut and migrate on its outer surface toward the mesoderm, where they eventually associate with the somatic tissues of the gonad. Here we demonstrate that the exit and migration are specific behaviors of the primordial germ cells and that they are controlled by the somatic tissue of the embryo rather than by a germ cell autonomous clock. Using mutations, we show that these controlling somatic events probably occur in the tissue of the gut primordium itself.

scholarly journals CFTR is required for the migration of primordial germ cells during zebrafish early embryogenesis

Reproduction ◽  
2018 ◽  
Vol 156 (3) ◽  
pp. 261-268 ◽  
Author(s):  
Huijuan Liao ◽  
Yan Chen ◽  
Yulong Li ◽  
Shaolong Xue ◽  
Mingfeng Liu ◽  
...  
Keyword(s):  
Germ Cell ◽  
Germ Cells ◽  
Primordial Germ Cells ◽  
Cell Development ◽  
Early Embryo ◽  
Early Embryogenesis ◽  
Key Factors ◽  
Zebrafish Model ◽  
Germ Cell Development

Mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene affect fertility in both sexes. However, the involvement of CFTR in regulating germ cell development remains largely unknown. Here, we used zebrafish model to investigate the role of CFTR in primordial germ cells (PGCs) development. We generated a cftr frameshift mutant zebrafish line using CRISPR/Cas9 technique and investigated the migration of PGCs during early embryo development. Our results showed that loss of Cftr impairs the migration of PGCs from dome stages onward. The migration of PGCs was also perturbed by treatment of CFTRinh-172, a gating-specific CFTR channel inhibitor. Moreover, defected PGCs migration in cftr mutant embryos can be partially rescued by injection of WT but not other channel-defective mutant cftr mRNAs. Finally, we observed the elevation of cxcr4b, cxcl12a, rgs14a and ca15b, key factors involved in zebrafish PGCs migration, in cftr-mutant zebrafish embryos. Taken together, the present study revealed an important role of CFTR acting as an ion channel in regulating PGCs migration during early embryogenesis. Defect of which may impair germ cell development through elevation of key factors involved in cell motility and response to chemotactic gradient in PGCs.

scholarly journals Proliferation and migration of primordial germ cells in We/We mouse embryos

1993 ◽  
Vol 198 (3) ◽  
pp. 182-189 ◽  
Author(s):  
Mia Buehr ◽  
Anne McLaren ◽  
Aine Bartley ◽  
Susan Darling
Keyword(s):  
Germ Cells ◽  
Primordial Germ Cells ◽  
Mouse Embryos ◽  
And Migration ◽  
Proliferation And Migration

scholarly journals Primordial Germ Cell Specification and Migration

F1000Research ◽  
2015 ◽  
Vol 4 ◽  
pp. 1462 ◽  
Author(s):  
Florence Marlow
Keyword(s):  
Germ Cell ◽  
Germ Cells ◽  
Primordial Germ Cells ◽  
Primordial Germ Cell ◽  
Gene Products ◽  
Cell Specification ◽  
Zygotic Transcription ◽  
Germ Cell Specification ◽  
And Migration ◽  
Insight Into

Primordial germ cells are the progenitor cells that give rise to the gametes. In some animals, the germline is induced by zygotic transcription factors, whereas in others, primordial germ cell specification occurs via inheritance of maternally provided gene products known as germ plasm. Once specified, the primordial germ cells of some animals must acquire motility and migrate to the gonad in order to survive. In all animals examined, perinuclear structures called germ granules form within germ cells. This review focuses on some of the recent studies, conducted by several groups using diverse systems, from invertebrates to vertebrates, which have provided mechanistic insight into the molecular regulation of germ cell specification and migration.

Tissue non-specific alkaline phosphatase is expressed in both embryonic and extraembryonic lineages during mouse embryogenesis but is not required for migration of primordial germ cells

Development ◽  
1995 ◽  
Vol 121 (5) ◽  
pp. 1487-1496 ◽  
Author(s):  
G.R. MacGregor ◽  
B.P. Zambrowicz ◽  
P. Soriano
Keyword(s):  
Alkaline Phosphatase ◽  
Germ Cell ◽  
Germ Cells ◽  
Primordial Germ Cells ◽  
Primordial Germ Cell ◽  
Embryonic Stem ◽  
Blastocyst Stage ◽  
Early Embryo ◽  
Specific Alkaline Phosphatase

Mouse primordial germ cells express tissue non-specific alkaline phosphatase (TNAP) during development, but the widespread expression of another alkaline phosphatase gene in the early embryo limits the potential use of this marker to trace germ cells. To attempt to identify germ cells at all stages during embryonic development and to understand the role of TNAP in germ cell ontogeny, mice carrying a beta geo (lacZ/neor) disrupted allele of the TNAP gene were generated by homologous recombination in embryonic stem cells. Using beta-galactosidase activity, the embryonic pattern of TNAP expression was examined from the blastocyst stage to embryonic day 14. Results indicate that primordial germ cell progenitors do not express TNAP prior to gastrulation although at earlier times TNAP expression is found in an extraembryonic lineage destined to form the chorion. In homozygous mutants, primordial germ cells appear unaffected indicating that TNAP is not essential for their development or migration.

Steel factor controls midline cell death of primordial germ cells and is essential for their normal proliferation and migration

Development ◽  
2006 ◽  
Vol 133 (24) ◽  
pp. 4861-4869 ◽  
Author(s):  
C. Runyan ◽  
K. Schaible ◽  
K. Molyneaux ◽  
Z. Wang ◽  
L. Levin ◽  
...  
Keyword(s):  
Cell Death ◽  
Germ Cells ◽  
Primordial Germ Cells ◽  
Steel Factor ◽  
And Migration ◽  
Proliferation And Migration

scholarly journals miR-636 inhibits EMT, cell proliferation and cell cycle of ovarian cancer by directly targeting transcription factor Gli2 involved in Hedgehog pathway

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Jiong Ma ◽  
Chunxia Zhou ◽  
Xuejun Chen
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Protein Expression ◽  
Signaling Pathway ◽  
Luciferase Reporter ◽  
Cell Proliferation And Migration ◽  
Hh Signaling ◽  
And Migration ◽  
Proliferation And Migration

Abstract Background Hedgehog (Hh) signaling pathway, which is essential for cell proliferation and differentiation, is noted to be aberrantly activated in tumor from increasing studies in recent years. MicroRNAs (miRNAs) as an important non-coding RNA in cells have been proven to possess a regulatory role specific to the Hh signaling pathway. Here, in vitro and in vivo cellular/molecular experiments were adopted to clarify the regulatory mechanism linking miR-636 to the Hh signaling pathway in ovarian cancer (OVC). Methods Protein–protein interaction analysis was performed to identify the hub gene in the Hh pathway. TargetScan database was used to predict the potential upstream regulators for Gli2. qRT-PCR was performed to test the expression of miR-636, while Western blot was conducted to detect the expression of proteins related to the Hh pathway and epithelial-mesenchymal transition (EMT). For cell functional experiments, HO-8910PM OVC cell line was used. MTT assay and wound healing assay were used to measure the effect of miR-636 on cell proliferation and migration. Flow cytometry was carried out to examine the effect of miR-636 on cell cycle, and Western blot was used to identify the change in expression of Hh and EMT-related proteins. Dual-luciferase reporter gene assay was implemented to detect the targeting relationship between miR-636 and Gli2. Xenotransplantation models were established for in vivo examination. Results Gli2 was identified as the hub gene of the Hh pathway and it was validated to be regulated by miR-636 based on the data from TargetScan and GEO databases. In vitro experiments discovered that miR-636 was significantly lowly expressed in OVC cell lines, and overexpressing miR-636 significantly inhibited HO-8910PM cell proliferation, migration and induced cell cycle arrest in G0/G1 phase, while the inhibition of miR-636 caused opposite results. Dual-luciferase reporter gene assay revealed that Gli2 was the target gene of miR-636 in OVC. Besides, overexpressed miR-636 decreased protein expression of Gli2, and affected the expression of proteins related to the Hh signaling pathway and EMT. Rescue experiments verified that overexpression of Gli2 reversed the inhibitory effect of miR-636 on HO-8910PM cell proliferation and migration, and attenuated the blocking effect of miR-636 on cell cycle. The xenotransplantation experiment suggested that miR-636 inhibited cell growth of OVC by decreasing Gli2 expression. Besides, overexpressing Gli2 potentiated the EMT process of OVC cells via decreasing E-cadherin protein expression and increasing Vimentin protein expression, and it reversed the inhibitory effect of miR-636 on OVC cell proliferation in vivo. Conclusion miR-636 mediates the activation of the Hh pathway via binding to Gli2, thus inhibiting EMT, suppressing cell proliferation and migration of OVC. Trial registration: The experimental protocol was established, according to the ethical guidelines of the Helsinki Declaration and was approved by the Human Ethics Committee of The Second Affiliated hospital of Zhejiang University School of Medicine (IR2019001235). Written informed consent was obtained from individual or guardian participants.

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