Primary and Secondary Mesenchyme Cells

Primary Mesenchyme Cells (PMCs)
Primary mesenchyme cells become important during gastrulation. They ingress when the embryo is a blastula. They do this through the use of slender filopodia to maintain contact with the basal lamina [1]. They rearrange until they form a ring-like structure, just below the equator of the embryo. How the PMCs reach their formation has been a question under research.

Figure 1: A L. variegatus mesenchyme blastula, viewed from the side, showing ingressing primary, or skeletogenic, mesenchyme cells (PMCs) [2].

PMCs are typically located at the vegetal hemisphere when the organism is in a blastocoel stage. In one experiment, tagged PMCs where microinjected into the animal region. The cells migrated to the correct sites in the vegetal region [3]. There was a control of latex beads and other cell types being inserted instead, and they did not show similar movements. These results lead to the conclusion that PMCs have some receptors that allow them to receive cues from the environment about where they should be located. An additional experiment that tested if PMCs were controlled by environmental factors, was when cells were treated with nickel chloride [4]. Nickel chloride abolishes the bilateral symmetry, and causes an overproduction of ventral ectoderm and an underproduction of dorsal ectoderm. It also causes the ciliated band, which separates ventral from dorsal to become ventral. In these cells, the skeleton pattern the PMCs is highly disturbed; it becomes radicalized. See Figure 2. However, nickel chloride affected individuals can still control size and have some pattern regulation. Figure 2: A radicalized and a typical skeleton. [4]

They also transferred PMCs from an individual without the nickel treatment into an individual with the nickel treatment. The skeleton was still radicalized. When PMCs from an individual treated with nickel chloride were transferred to an individual that was not treated with nickel chloride the normal bilateral skeleton was formed [4]. This experiment offers strong evidence that there are external environmental cues that help control the migration of PMCs; however, PMCs do have some innate abilities, such as controlling size.

Another experiment was performed where PMCs were removed or extra PMCs were added to see the effects of quantity on signaling [1]. The researchers observed if the PMCs distributed in the same proportions they would normally. When there was a shortage of PMCs, they were expected to congregate in preferred locations. The results showed that whether there was a typical number of PMCs or a shortage, the PMCs distributed in relatively the same proportions. See Table 1. This leads to the conclusion that PMCs do not prefer a certain location, nor do they compete with each other for locations. Also, when there was a reduced number of PMCs, the embryo continued to develop normally. These observations lead to the conclusion that development is independent of the quantity of PMCs [1].

Table 1: The distribution of PMCs depending on density[1].

There were experiments performed where there was an increase in the number of PMCs [1]. These experiments could not give the quantitative results of the previous experiments due to difficulties in counting the increased numbers, but much of the same pattern was seen. In most cases, the excess PMCs stayed attached to the blastocoel wall, but in some cases where there was an extreme increase were PMCs found scattered throughout the cell. The excess PMCs were labeled and found to incorporate in all parts of the normal patterning. No PMCs appear to switch fate due to overcrowding. These results show that there is an upper limit of which an organism can handle PMCs, but a moderate increase can be handled and incorporated into the organism’s normal structures [1].

Another experiment tested whether individual PMCs were fated for certain parts of the pattern or if they were all equivalent [1]. This was done through two separate experiments. In the first one the organism was allowed to develop to the midgastrula stage. Then PMCs were labeled and moved to the blastocoels of a mesenchyme blastula. The results showed that the cells were able to contribute to parts of the pattern that they were not originally a part. In the second experiment, PMCs were taken from an earlier stage blastula and microinjected into a later stage blastula. These cells incorporated into the pattern successfully [1]. The experiments are strong evidence that all PMCs are equivalent and have the possibility of being any part of the pattern. The patterning of PMCs is a combination of environmental factors and the capabilities that are ingrained in the cell [1].

Secondary Mesenchyme Cells (SMCs)

Figure 3: The locations of SMCs. SMCs create filopodia that explore the blastocoels by extending, attempting attachment, and retracting when they do not find a suitable location. [4]

First, they must migrate to become associated with the archenteron, and then they start stretching trying to find the animal pole. How they originally migrate to the archenteron is still a question, but there are four main hypotheses.
1. Differences in surface topography
2. Tissue proximity
3. Tissue curvature
4. The ventral ectoderm is more adhesive

Once the SMCs are attached to the archenteron, the filopodia begin to extend trying to find their target location. The filopodia that reach the apical plate, by the animal pole, tend to stay attached for 20-50 times as long. As more filopodia become attached, the archenteron becomes closer and more filopodia find their target destination. When the animal pole is manipulated closer to the filopodia development occurs faster. When the filopodia are separated and unable to reach the animal pole, SMCs will detach and find the animal pole [4].

1. Ettensohn, C.A., The regulation of primary mesenchyme cell patterning. Developmental Biology, 1990. 140(2): p. 261-271.
2. Available from:
3. Ettensohn, C.A. and D.R. McClay, The regulation of primary mesenchyme cell migration in the sea urchin embryo: transplantations of cells and latex beads. Dev Biol, 1986. 117(2): p. 380-91.
4. Hardin, J., Target Recognition by Mesenchyme Cells during Sea Urchin Gastrulation. American Zoologist, 1995. 35(4): p. 358-371.

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