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A mutational analysis of multicellular development.

作者信息

Carrin Ines, Murgia Irene, McLachlan Andrew, Kay Robert R

机构信息

MRC Laboratory of Molecular Biology, Hills Road, Cambridge CB2 2QH, UK.

出版信息

Microbiology (Reading). 1996 Apr;142(4):993-1003. doi: 10.1099/00221287-142-4-993.

DOI:10.1099/00221287-142-4-993
PMID:33725786
Abstract

We have collected mutants that arrest in development after aggregation, but before first finger formation. A total of 118 mutant strains were isolated and are referred to as mound mutants. Nine complementation groups , containing 46 of the mutant strains, were defined by parasexual methods. A statistical analysis suggested that there are about 118 genes which, when mutated, confer the mound phenotype. Of these genes, about 60 are predicted to be mutated in our collection: the 9 assigned to complementation groups and another 51 unassigned mutants. and were assigned to linkage groups VII, IV, II and VI, respectively. Development of the mutant strains was characterized by terminal morphology, neutral red staining and expression of marker mRNAs for prespore and prestalk cells. Three broad classes were recognized. (1) Postaggregative mutants - those blocked early in multicellular development. They did not express any of the prestalk or prespore marker mRNAs and generally arrested as low mounds or ridges. (2) Pathway mutants - those blocked specifically in either prestalk or prespore differentiation. They expressed either prestalk or prespore marker mRNAs, but not both, and generally proceeded further morphologically than post-aggregative mutants. (3) Morphogenesis mutants - those apparently blocked in morphogenesis rather than cell differentiation. They expressed all the cell-type marker mRNAs tested. Most arrested as tight mounds lacking a tip and of defined upper size, but some mutants produced aberrant tips. The majority of mutants tested synergized with wild-type: 24/28 strains which cannot make spores when developed alone, were able do so when allowed to develop with an equal number of wild-type cells. We suggest that some of the morphogenesis mutants have a cytoskeletal defect which prevents first finger formation and that these mutants can be physically carried through development by the wildtype (synergy by 'piggy-backing').

摘要

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