By today's standards and for any particular cell to claim an identity, it has to be a molecular one. Until a molecular definition of the "primordial germinal layer' is put forward there's no way to trace it in molecular terms or establish its lineage. Another way is to label an embryo with 3 lineage specific tracers, say, EGFP driven by a ectodermal promoter, LacZ driven by a mesoderm promoter, and luciferase driven by an endoderm promoter. So let say that we harvest embryos at different times and develop all markers (EGFP, LacZ and Luciferase) in all specimens. Let's say that there's a group of cells that don't express any of them. Assuming there is complete expression, the label-excluding cell group would fit the definition of PGCs (layer-less) with that particular assay. Alternatively, if all cells are labeled with a particular marker or even show multiple markers, then marker leakage is an explanation or the so-called PGC doesn't exist. There are other labeling approaches like the limited diluted retroviral infection by Connie Cepko. My take.

From Saitou et al., Development, 2012 on mouse PGCs:

"PGC specification takes place in the most proximal epiblast in response to bone morphogenetic protein (BMP) signalling from the extra-embryonic ectoderm at ∼E6.0 (Lawson et al., 1999) (Fig. 2A,B). At this stage, epiblast cells are still pluripotent but are being propelled towards somatic fates and are in the process of losing their pluripotency (Kurimoto et al., 2008)."

Today's standards for tracking stem cell fate in organismal systems are higher than simply a molecular one.  We impose standards on what we produce.  So, why don't we have common standards?

For example, should we want to track cell behaviors and know molecular information at the same time? 

This topic is exciting and so I decided to read more because it has changed a lot since I last reviewed it many years ago. Primordial Germ Cells (PGC) as Jerry Rhee points out come from the epiblast, an embryonic structure preceding the 3-layer embryo. These cells are unique because they will end up forming the gametes in both males and females but also because the have a characteristic program of development. Erez Raz's review in Nature Genetics in 2003 is very telling about the migration pattern in zebrafish embryos; and how a particular RNA marker (the VASA gene) defines its identity plus the Raz paper mentions additional markers. - Diego Castrillon's PNAS paper from 2000 shows that the VASA gene marker is expressed in adult tissues but also serves as an ideal marker for the PGCs since it's not expressed in other early somatic cells that belong to the ectoderm, mesoderm and endoderm. It's conserved in many species including humans. So I think Gnanasekaran's question is very motivating and now we can conclude that definitely PGCs can be traced to the epiblast, they exist, and have unique markers like the VASA gene to allow the cell and molecular tracing.   Maria de Miguel's paper in Int. J. Dev. Biol. 53: 1529-1540 (2009) has good explanations and summary figures. 

Oct4 is a good molecular marker for primary germ cells.  Actually they do have a history of migration.  At the time of gastrulation in the mouse, most PGCs are not actually in the embryo proper, they are in the posterior region near the extraembryonic tissue that is forming the allantois.   The PGCs then migrate rostrally between the endoderm and mesoderm, eventually settling in the gonadal ridge.

Hi My colleagues.

There is a chapter can help people understand a little more about the PGCs. Hopefully help everyone.

Somehow we have switched from the role of the three primordial germ layers of the gastrula into the origin of the germ cells.

I was trying to ask you to evaluate the evidence that the three primordial germ layers are the lineal precursors of specific tissue types such as epithelia , mesenchyme, heamatoleukopoietic cells etc.

This might be contrasted with a model in which stem cell lineages create domains of epithelial and mesenchymal cells locally.

Are tumors monoclonal? How do we know? Are the mesenchymal portions of tumors part of the same colony as the epithelial portions?

epithelium and mesenchyme are not really what i would call "cell types".  They are morphological descriptions of cells or cell groups with varying degrees of adhesion and shared orientation.  For example, a pseudo-epithelium is a kind-of epithelium in which cells are attached as a cluster and show some degree of polarity but not quite mesenchymal and individuated.  Moreover, there can be different types of cells within a single epithelial monolayer.

The nomenclature of stem cells is a bit confusing and so the chapter that Thao Huynh duy shared is very helpful. In it, you can find the following description for PGCs "a population of cells near the epiblast (Figure 2.1) can be identified as primordial germ cells (PGCs), which are subsequently excluded from somatic specification or restriction. PGCs migrate to and colonize the genital ridges, where they produce mature germ cells and generate functional adult gametes". So technically, PGCs end up forming gametes although a deeper look at the literature will suggest that these cells can be skewed into forming say, hematopoietic tissues (Maria de Miguel's paper cited above).  -

I believe the evidence shows that adult tissues do come from their respective layers but in development, cells from one embryonic layer intermingle within the guts of the other layer, an example that I provided earlier was the migration of ectodermally-derived neural crest cells into endoderm-derived cells as argued below

Adult tissues are composed from cells that arise from multiple layers. In the example of the colon, it's been demonstrated through very elegant approaches like the chick-quail chimeras as well as the lineage tracing retroviral studies of Constance Cepko that ectodermally-derived neural crest cells migrate and end up forming local neurons and ganglia throughout the whole gastrointestinal tract. One example for such mechanism is Hirchsprung's disease in which mesenteric ganglia don't develop (neurons don't arrive from the neural crest) and thus the large intestine lacks peristalsis or tonic movements and thus fecal matter has trouble to exit the intestine causing constipation, intestinal obstruction, and eventual enlargement of the intestine. But examples like this are abundant in other organs like the cells that make up the pacemaker in the heart or the pressure control organs in the large vessels are also derived from the neural crest.

Regarding tumors, it's believed that these are initially monoclonal from the stage for INITIATION and PROMOTION but once they undergo the transformation stage like for example becoming anchorage-independent, they might undergo diversification through a process called TUMOR EVOLUTION that allow them to mutate new driver genes (oncogenes and antioncognes), cause genomic instability (as seen with passenger genes) and rapid adaptation to drugs, for example. In other words, once they start to evolve they become polyclonal, they will be more so if part of the tumor metastasizes and continues evolving in a new location.  Because tumor secrete paracrine and autocrine mediators they influence their surroundings which might change although they might not be tumorigenic, they're simply responding to the tumor's milieu (seed or soil hypothesis).