Abnormal cytoskeletal and chromosome distribution in po, ms4 and ms6; mutant alleles of polymitotic that disrupt the cell cycle progression from meiosis to mitosis in maize.

The maize cell cycle regulation mutant polymitotic (po) progresses through abnormal cell cycles, characterized by premature cell divisions without chromosome duplication of the daughter cells produced by meiosis during microsporogenesis and macrosporogenesis. There are three recessive alleles of the Po gene; po, ms4, and ms6. A new method of permeabilizing cells based on freeze-fracture technology was used to study the distribution of microtubules in wild-type and mutant microspores. Here we show that an abnormal distribution of microtubules is correlated with changes in chromosome morphology in a cell cycle-dependent manner in po, ms4 and ms6 mutant alleles. After meiosis II, the cell cycle is complete and becomes progressively less synchronous in po homozygotes compared with wild-type cells. During microsporogenesis, the distribution of microtubules is abnormal, and chromosome morphology is altered in both po, ms4 and ms6 mutants. However, more chromosome fragments or micronuclei associated with minispindles are present in ms6 than po and ms4. After microspores are released from the tetrads, disruptions in structure and organization of chromosomes and microtubules continues in subsequent abnormal cell cycles. However, these cell cycles are incomplete since phragmoplasts are not formed. During these incomplete cell cycles, abnormal spindles and microtubule arrays are induced and extra microtubule arrays are associated with irregularly distributed chromosome fragments. States corresponding to interphase, prophase, metaphase and anaphase can be recognized in the mutant microspores. Abnormal cell cycles also occur after female meiosis during ms4 macrospore development. Since only the cell that normally undergoes embryo sac development (the chazal-most cell) undergoes supernumerary divisions this suggests that the po phenotype can be characterized as premature haploid divisions rather than repetition of meiosis II.