50 Hz magnetic fields of varying flux intensity affect cell shape changes in invertebrate immunocytes: The role of potassium ion channels

2002 ◽  
Vol 23 (4) ◽  
pp. 292-297 ◽  
Author(s):  
Enzo Ottaviani ◽  
Davide Malagoli ◽  
Alex Ferrari ◽  
Davide Tagliazucchi ◽  
Angela Conte ◽  
...  
Keyword(s):  
Ion Channels ◽  
Magnetic Fields ◽  
Cell Shape ◽  
Potassium Ion ◽  
Potassium Ion Channels ◽  
Flux Intensity ◽  
Cell Shape Changes ◽  
Shape Changes

Second-Site Noncomplementation Identifies Genomic Regions Required for Drosophila Nonmuscle Myosin Function During Morphogenesis

Genetics ◽  
1998 ◽  
Vol 148 (4) ◽  
pp. 1845-1863
Author(s):  
Susan R Halsell ◽  
Daniel P Kiehart
Keyword(s):  
Cell Shape ◽  
Myosin Ii ◽  
Nonmuscle Myosin ◽  
Genetic Screens ◽  
Nonmuscle Myosin Ii ◽  
Cell Shape Changes ◽  
Genomic Regions ◽  
Shape Changes ◽  
Strong Interactors

Abstract Drosophila is an ideal metazoan model system for analyzing the role of nonmuscle myosin-II (henceforth, myosin) during development. In Drosophila, myosin function is required for cytokinesis and morphogenesis driven by cell migration and/or cell shape changes during oogenesis, embryogenesis, larval development and pupal metamorphosis. The mechanisms that regulate myosin function and the supramolecular structures into which myosin incorporates have not been systematically characterized. The genetic screens described here identify genomic regions that uncover loci that facilitate myosin function. The nonmuscle myosin heavy chain is encoded by a single locus, zipper. Contiguous chromosomal deficiencies that represent approximately 70% of the euchromatic genome were screened for genetic interactions with two recessive lethal alleles of zipper in a second-site noncomplementation assay for the malformed phenotype. Malformation in the adult leg reflects aberrations in cell shape changes driven by myosin-based contraction during leg morphogenesis. Of the 158 deficiencies tested, 47 behaved as second-site noncomplementors of zipper. Two of the deficiencies are strong interactors, 17 are intermediate and 28 are weak. Finer genetic mapping reveals that mutations in cytoplasmic tropomyosin and viking (collagen IV) behave as second-site noncomplementors of zipper during leg morphogenesis and that zipper function requires a previously uncharacterized locus, E3.10/J3.8, for leg morphogenesis and viability.

scholarly journals Transcriptional regulation of cell shape during organ morphogenesis

2018 ◽  
Vol 217 (9) ◽  
pp. 2987-3005 ◽  
Author(s):  
Aravind Sivakumar ◽  
Natasza A. Kurpios
Keyword(s):  
Transcriptional Regulation ◽  
Cell Shape ◽  
Evolutionary Conservation ◽  
Model Organisms ◽  
Critical Question ◽  
Organ Morphogenesis ◽  
Open Questions ◽  
Cell Shape Changes ◽  
Shape Changes

The emerging field of transcriptional regulation of cell shape changes aims to address the critical question of how gene expression programs produce a change in cell shape. Together with cell growth, division, and death, changes in cell shape are essential for organ morphogenesis. Whereas most studies of cell shape focus on posttranslational events involved in protein organization and distribution, cell shape changes can be genetically programmed. This review highlights the essential role of transcriptional regulation of cell shape during morphogenesis of the heart, lungs, gastrointestinal tract, and kidneys. We emphasize the evolutionary conservation of these processes across different model organisms and discuss perspectives on open questions and research avenues that may provide mechanistic insights toward understanding birth defects.

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