Development, Vol 120, Issue 3 591-601, Copyright © 1994 by Company of Biologists

JOURNAL ARTICLES

Aberrant pattern formation in myosin heavy chain mutants of Dictyostelium

D. Traynor, M. Tasaka, T. Takeuchi and J. Williams

In mutant Dictyostelium strains that fail to accumulate the myosin heavy chain (MHC A), development is relatively normal up to the tight aggregate stage but is arrested prior to formation of the apical tip (DeLozanne and Spudich 1987, Knecht and Loomis, 1987). We show that in aggregates formed by such MHC A deficient (MHC A-) strains the proportions of pstA and pstB cells, the two prestalk cell types, and of prespore cells are similar to those found during normal development but their distribution is radically different. During the initial stages of normal slug formation, pstA cells move to the tip, pstB cells accumulate in the base and prespore cells occupy the remainder of the aggregate. In the aggregates initially formed by MHC A- mutants pstA cells are present in a central core, pstB cells are present in the cortex and prespore cells lie sandwiched between them. Eventually, cells within the cortex differentiate into mature stalk cells but spores are never formed. Mixing experiments, in which MHC A- cells are allowed to co-aggregate with an excess of normal cells, show that MHC A- prestalk cells enter the aggregate relatively normally but are unable to enter the slug tip or to migrate into the stalk at culmination and that MHC A- prespore cells accumulate in the lower part of the spore head during culmination. Thus MHC A- cells appear to be able to move within the multicellular aggregate but are incapable of participating in normal morphogenesis. The structures formed by MHC A- cells are very similar to those of the agglomerates that form when wild-type cells are developed in roller-tube culture, conditions that result in loss of the polarity imparted by the presence of an air-water interface. We propose formation of such a structure by MHC A- cells to be a default response, caused by their inability to undertake the shape changes and intercalatory cell movements that are necessary to form and extend the tip.
CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter    What's this?

This article has been cited by other articles:

				M. C. Mendoza, F. Du, N. Iranfar, N. Tang, H. Ma, W. F. Loomis, and R. A. Firtel Loss of SMEK, a Novel, Conserved Protein, Suppresses mek1 Null Cell Polarity, Chemotaxis, and Gene Expression Defects Mol. Cell. Biol., September 1, 2005; 25(17): 7839 - 7853. [Abstract] [Full Text] [PDF]

				K. Yoshida and K. Inouye Myosin II-dependent cylindrical protrusions induced by quinine in Dictyostelium: antagonizing effects of actin polymerization at the leading edge J. Cell Sci., January 6, 2001; 114(11): 2155 - 2165. [Abstract] [Full Text] [PDF]

				S. Chien, C. Y. Chung, S. Sukumaran, N. Osborne, S. Lee, C. Ellsworth, J. G. McNally, and R. A. Firtel The Dictyostelium LIM Domain-containing Protein LIM2 Is Essential for Proper Chemotaxis and Morphogenesis Mol. Biol. Cell, April 1, 2000; 11(4): 1275 - 1291. [Abstract] [Full Text]

				P. Clow, T Chen, R. Chisholm, and J. McNally Three-dimensional in vivo analysis of Dictyostelium mounds reveals directional sorting of prestalk cells and defines a role for the myosin II regulatory light chain in prestalk cell sorting and tip protrusion Development, January 6, 2000; 127(12): 2715 - 2728. [Abstract] [PDF]

				P. A. Clow and J. G. McNally In Vivo Observations of Myosin II Dynamics Support a Role in Rear Retraction Mol. Biol. Cell, May 1, 1999; 10(5): 1309 - 1323. [Abstract] [Full Text]

				T. Chen, W. Wolf, and R. Chisholm Cell-type-specific rescue of myosin function during Dictyostelium development defines two distinct cell movements required for culmination Development, January 10, 1998; 125(19): 3895 - 3903. [Abstract] [PDF]

				F Rivero, B Koppel, B Peracino, S Bozzaro, F Siegert, C. Weijer, M Schleicher, R Albrecht, and A. Noegel The role of the cortical cytoskeleton: F-actin crosslinking proteins protect against osmotic stress, ensure cell size, cell shape and motility, and contribute to phagocytosis and development J. Cell Sci., January 11, 1996; 109(11): 2679 - 2691. [Abstract] [PDF]

				T. Chen, P. Kowalczyk, G Ho, and R. Chisholm Targeted disruption of the Dictyostelium myosin essential light chain gene produces cells defective in cytokinesis and morphogenesis J. Cell Sci., January 10, 1995; 108(10): 3207 - 3218. [Abstract] [PDF]

				E Shelden and D. Knecht Mutants lacking myosin II cannot resist forces generated during multicellular morphogenesis J. Cell Sci., January 3, 1995; 108(3): 1105 - 1115. [Abstract] [PDF]