Cellular mechanisms of nuclear migration


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Resumo

Subcellular mobility, positioning, and directional movement of the nucleus in a certain site of the cell or cenocyte and, less frequently, intercellular translocation of the nucleus accompany the cell and tissue differentiation, change of their functions, and the organism growth and development and its response to stress, plant–microbial interactions, symbiosis, and many other processes in plants and animals. The nucleus movement is performed and directed through the interaction between dynamic cytoskeleton components and nucleus by means of signal-binding proteins, including motor and linker. The cell responds to the external signal by mobilization and polar reconstruction of the cytoskeleton components, as a result of which the nucleus displacement by means of actomyosin or microtubule mechanisms in cooperation with dynein and kinesin occurs. In plants, the actomyosin mechanism is involved in the nucleus migration; it allows the nucleus to move rapidly and over significant distances in response to environmental stimuli. An important role in the nucleus translocation belongs to the linker complexes of the proteins that are inserted in the nuclear envelope, that connect and transmit signals from the plasmalemma to the cytoplasm and nucleoplasm, and that provide the skeletal basis for many subcellular compartments. Changes in the protein composition, conformational modifications of the proteins, and displacement of linkers from the nuclear envelope result in the nucleus detachment from the cytoskeleton, and change in the form, mechanical rigidity, and positioning of the nucleus.

Sobre autores

E. Kravets

Institute of Food Biotechnology and Genomics

Autor responsável pela correspondência
Email: kravetshelen@gmail.com
Ucrânia, Kyiv

A. Yemets

Institute of Food Biotechnology and Genomics

Email: kravetshelen@gmail.com
Ucrânia, Kyiv

Ya. Blume

Institute of Food Biotechnology and Genomics

Email: kravetshelen@gmail.com
Ucrânia, Kyiv


Declaração de direitos autorais © Allerton Press, Inc., 2017

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