Cell migration

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Under cell migration ( Latin. Migrare 'wander) is the active locomotion (locomotion) of cells or cell aggregates. The umbrella term "migration" includes the non-directional spontaneous movement ( random migration ), the directed, chemotactic movement and the change in the speed of movement (chemokinetics). Within a metazoic organism, only certain cells are able to migrate: embryonic cells, and in the mature organism certain cell types of the connective tissue , the vessels, some epithelia , tumor cells and, to a particularly high degree, the cells of the immune system and the sperm . In prokaryotic organisms, migration takes place with the help of flagella and cilia .

Locomotion by means of flagella and cilia

Sperm move by means of a flagellum ( flagellum ) and need open areas of liquid. Many prokaryotes also provide flagella with the necessary motility , but the structure of the prokaryotic flagella is completely different from that of eukaryotes. Cilia are found exclusively in eukaryotic cells. The most prominent examples using cilia to move cells freely are paramecia and ciliates ( ciliates ).

Amoeboid movement

For body cells that migrate in the confines of the tissue structures, the amoeboid movement is advantageous because it enables considerable deformation and adaptation to the existing spatial conditions. Many eukaryotic cells, such as fibroblasts , keratinocytes , neurons , immune cells and of course amoeba, are able to migrate through amoeboid movement.

The amoeboid movement is essentially based on the dynamic reshaping of two cell structures and on the attachment to the extracellular matrix: on the extension of fibrillary proteins ( actin ) and the incorporation of membrane vesicles in the direction of movement, which results in the formation of cell processes ( filopodia and lamellipodium ) . In lamellipodia and filopodia, a structure of high molecular weight, fibrillar F-actin builds up, which continues to grow at the front edge through the addition of low molecular weight G-actin, while it breaks down into G-actin again at its rear side (so-called treadmilling ). At the same time, the front edge of the lamellipodium is expanded by the incorporation of membrane material that comes from the cell's own vesicles. These vesicles are transported forward along another fibrillar structure, the microtubules . In this way, the actin framework moves into the sack of the lamellipodium, which advances through the installation of new membrane material. Meanwhile probe filopodia, driven also by growing actin filaments, at the front of Leitsaums ( leading edge ) the environment for suitable conditions for adhesion to the substrate. Focal complexes of the filopodia ( filopodial focal complexes ) then make the first contact with the extracellular matrix (ECM), whereby stable focal contacts are formed as the cell advances further in the lamellipodium .

With the vesicles, membrane-bound receptors for chemotaxins and growth factors, as well as adhesive proteins with which the cell attaches itself to its base, and other types of receptors are built into the front of the migrating cell and are constantly being supplemented. The actin framework, which is held together by various cross-linking proteins, connects to these receptors and provides lamellipodia and filopodia with stability and the propulsion necessary for migration. Depending on the cell type, the vesicles also release enzymes and oxygen radicals to the outside when they are incorporated, which loosen the tissue and thus facilitate cell movement (“enzymatic machete”). The membrane material, which is constantly being built into the front of the lamellipodium, gradually migrates to the rear of the cell, where it is drawn in together with the receptors in the form of vesicles, which are regenerated in the Golgi apparatus and transported forward again to allow further progress of lamellipodia and filopodia (membrane flow). At the same time, the actin framework contracts with the help of the motor protein myosin , which builds up a pressure within the cell that, due to the solar-like state of aggregation in the direction of movement (in contrast to the gel-like state of aggregation at the rear end of the cell), can only escape forwards. In this way, the back part of the cell is pulled along while the front part continues to expand. A cell migrating amoeboid thus moves in the desired direction by shifting and contracting its supporting and holding structure. The filopodia play a decisive role here, which by "scanning" the environment determine the formation, alignment and localization of focal contacts and thus also the direction of movement.

Cell migration tasks

The tasks of cell migration are diverse: shaping movements in the embryonic period and during growth; later structural transformation, regeneration, healing, etc. For the cells of the immune system it is important to find harmful material. The most agile immune cell is the neutrophil granulocyte , which with a resting diameter of around 7.5 µm can stretch up to 70 µm and wander through gaps down to 0.6 µm. Its migration speed is 10 to 20 µm per minute, depending on the conditions. The ability to migrate promotes metastasis of tumor cells .

See also


  • Claudia Schäfer The role of filopodia in adhesion formation during cell migration of keratinocytes
  • Gerd Egger, The acute inflammation , Springer 2005