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A budding figure BF is visible in the lower right corner. Haploid sperm S and residual bodies RB are also indicated. Abnormal budding figures are also present in which all the chromosomes remain in the center of the developing residual body. In the mat mutants, normal meiosis I—like spindles form, but anaphase figures are never observed F, G, J, and K. Given these striking differences between oocyte and spermatocyte meiosis, we investigated whether the mat genes functioned in both processes.

Testes from young adult mutant males, which had been upshifted to In contrast, mat mutant spreads exhibit a striking abundance of primary spermatocytes and sperm Fig. Notably, secondary spermatocytes are completely absent, and the DNA staining patterns suggest that meiosis in the mutant primary spermatocytes fails to progress past meiosis I.

Despite this apparent meiosis I arrest, cells that resemble haploid sperm still form, but they lack DNA which we refer to as anucleate. Similar sperm spreads were seen for most mat alleles data not shown under L3 shift-up conditions, with the striking exceptions that mat-3 or, or, and or and emb-1 hc62 and hc57 males produce morphologically normal secondary spermatocytes and haploid sperm and can sire viable offspring when mated to feminized hermaphrodites data not shown Sadler, P.

Fox, A. Pletcher, and D. Shakes, unpublished observations. As previously reported for emb and emb males Sadler and Shakes , affected mat-1 , mat-2 , and mat-3 males are unable to sire viable offspring, however, their anucleate sperm are surprisingly functional in that they can activate, crawl, and even fertilize oocytes.

To further understand the meiotic defects, we analyzed stage-specific DNA and tubulin structures in wild-type and mutant sperm spreads. In wild-type animals Fig.

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E , sperm spreads reveal a diversity of microtubule structures ranging from the large, closely opposed asters of the metaphase primary spermatocytes to the highly dynamic spindles of the secondary spermatocytes and budding figures. In mat mutants, including mat-2 ax Fig.

G , sperm spreads are dominated by large spermatocytes, each of which contains a metaphase array of chromosomes and a bipolar, astral, meiosis I metaphase spindle. In enlarged views Fig.

Some of the mutant spindles eventually elongate, but homologue separation and other anaphase events never occur. Thus, with the possible exception of emb-1 , whose two alleles lack spermatocyte defects, these data indicate that every mat gene is required for the meiosis I metaphase to anaphase transition in both oocytes and spermatocytes. Our analysis of oocyte and spermatocyte meiosis in the mutants suggested that the mat gene products function in a shared step of these two structurally dissimilar meiotic processes.

To address whether these mat genes function specifically to separate axially aligned homologues during meiosis I or whether they also function to separate sister chromatids during mitosis, we examined the mitotic divisions of germline nuclei within adults. Because germline mitotic divisions continue at a time when the animal's somatic cells have ceased to divide Beanan and Strome , they can be studied in adult upshifted mutants in the absence of potential complications from somatic defects.

When isolated wild-type gonads were immunostained with phosphohistone H3 antibodies, they were found to contain one to six mitotic germ cell nuclei in the distal region of each gonadal arm Fig. In an allele-specific manner, mutant gonads had either slightly or greatly elevated numbers of phospho-H3 staining mitotic germ cell nuclei Fig.

DAPI staining of these mitotic nuclei revealed that most of the phospho-H3—positive nuclei are in metaphase Fig. We believe that the excess in mitotic figures stems from an extended block or pause in metaphase, rather than an increased cell cycle rate, since upshifts of longer duration result in reduced rather than tumorous germlines data not shown.


Gonads were fixed and stained with the phospho-H3 antibody. Shown here is quantitation of the number of phospho-H3 positive germ cell nuclei per gonad arm. Phospho-H3 staining of adult upshifted wild-type A , mat-1 ax B , mat-2 ax C , and mat-3 or D hermaphrodites reveals an excess of mitotic plates in the mitotic region of germlines from isolated mutant gonads. Newly hatched C. To test whether mat genes are required for the initial expansion of the germline, mutants were upshifted as newly hatched L1 larvae.

For some alleles, the earlier upshift conditions did not significantly alter the mutant phenotype; these Mel adults had fully proliferated germlines and produced large broods of one-cell arrested embryos Table. For other alleles, these same conditions caused moderate to severe defects in germline proliferation Table and data not shown. In the most severe cases, L1 upshifts resulted in sterile Ste adults with fewer than 50 germ cells and no apparent gametes.

Similar defects in mitotic germline proliferation have been reported for null alleles of emb Furuta et al. Shown here are the 32 alleles recovered in the screen for the Mat phenotype. Also included are the previously existing alleles of emb g48 , emb g53 , and emb-1 hc57 and hc62 that belong in this class of Mat mutants. Shift-up experiments were also carried out with L1 larvae.

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Shift-up experiments with two-cell embryos were also carried out: most hatched and developed to the adult stage where they were either Mel or Ste. The phenotypes shown for the two-cell shift-ups represents the phenotypes of those embryos that hatched. For some alleles, a fraction of the embryos routinely die before hatching, regardless of the temperature conditions. In this table, the Ste category is broad, ranging from hermaphrodites with little or no germline to hermaphrodites that produce one or two embryos.

The three alleles listed at the bottom were isolated in the ts screen, but proved to be nonconditional upon outcrossing. To investigate whether the mat genes are also required for mitotic cell divisions of the soma, mutant hermaphrodites and males were upshifted as L1 larvae and examined for potential somatic defects. Although our analysis did not include all 32 alleles, we observed that a subset of alleles within the mat-1 , mat-2 , mat-3 , and emb complementation groups exhibit defects in somatic development.

Similar somatic defects were reported for a subset of emb alleles Furuta et al. For three mat-3 alleles, the animals are also uncoordinated, suggesting defects in the proliferation of cells that make up the ventral nerve cord. The hermaphrodite vulva, male tail, and ventral nerve cord are all structures that require substantial numbers of larval cell divisions, and the spectrum of observed phenotypes resemble those of cell cycle mutants in which postembryonic divisions have been disrupted O'Connell et al.

We have not yet determined whether these somatic defects are caused by arrest or delays in the mitotic cell cycle. Our complete set of ts alleles were tested in this manner, and, in most cases, these two-cell embryos underwent normal embryogenesis and developed into adults. Depending on the allele, the adults either produced broods of one-cell embryos Mel or were Ste Table. The unexpected mildness of the observed somatic defects, particularly in upshifted two-cell embryos, may suggest that these mat genes function in only a subset of mitotic divisions. Alternatively, our results may be explained by maternal rescue, gene redundancy, or the fact that these ts alleles are unlikely to be genetic nulls.

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Our premise, that these affected one-cell embryos reach a normal meiosis I metaphase state, but then fail to progress to anaphase, is supported by the following observations: a the oocytes undergo normal maturation events and, after fertilization, their chromosomes align and congress in a metaphase pentagonal array on a morphologically normal meiotic spindle, b in such embryos, the sperm chromatin remains condensed and the sperm microtubule organizing center remains quiescent, and c neither meiotic anaphase figures nor polar bodies are ever observed.

In addition, the stable presence of phosphohistone H3 and MPM-2 epitopes indicates that the mutant embryos are permanently arrested in an M phase—like state. These results suggest that functional meiotic CDKs drive the mutant embryos into metaphase of meiosis I, but because these CDKs are not subsequently deactivated, the mutant embryos are unable to transition out of a metaphase state. Importantly, the metaphase to anaphase transition defects in these mutants are not restricted to oocyte meiosis I.

Analogous defects are observed during spermatogenesis: primary spermatocytes undergo normal budding from the gonadal syncytium, undergo nuclear envelope breakdown, but then arrest in a normal meiosis I metaphase state and never form secondary spermatocytes. Thus, the same fundamental defect is seen in both spermatocyte and oocyte meiosis, despite the fact that spermatocytes employ astral, rather than anastral spindles.

On the other hand, the developmental consequences of this common meiosis I block are strikingly dissimilar. The mutant oocytes appear to be blocked from further development as their sperm chromatin remains condensed and their sperm-contributed microtubule organizing centers remain quiescent. In contrast, differentiation of the mutant spermatocytes proceeds with the eventual formation of motile, albeit anucleate, spermatozoa. These mutants also display metaphase to anaphase transition defects during mitosis.

Most dramatically affected are the mitotic divisions of proliferating germ cells; upshifted adults accumulate an excessive number of phospho-H3—staining germ cell nuclei, and upshifted larvae exhibit moderate to severe defects in germ cell proliferation. However, unlike the complete metaphase blocks observed during meiosis, the metaphase block during germ cell mitosis is frequently incomplete and results in an M phase delay.

The identification of defects in somatic tissues, such as the male tail and the hermaphrodite vulva, suggests that the mat genes are also required for mitotic divisions of the soma. Each of the mat genes, except for emb-1 , is represented by an allelic series that encompasses the full range of described metaphase to anaphase transition defects. Because identical mutant defects are observed in multiple alleles of multiple genes, they are likely to reflect important functions of this gene class.

Thus, our data implies that a common mechanism governs the transition from metaphase to anaphase, regardless of whether this transition a involves the separation of homologues or sister chromatids, b is mediated by anastral or astral spindles, c occurs within syncytial or nonsyncytial cells, or d involves germline or somatic cells. On the other hand, whereas all of the mutant alleles have defects in oocyte meiosis and most have defects in spermatocyte meiosis, many fewer exhibit defects in the mitotic divisions of either the germline or soma. Furthermore, we observed strong metaphase blocks during meiosis I, but primarily M phase delays during germline mitosis.

Thus, whereas the mat genes are required for all of these various cell divisions, meiotic divisions may be particularly sensitive to low levels of gene product. Alternatively, the design of our mutant screens may have favored the isolation of mutants with lesions in meiotic-specific or germline-specific domains. Sequence analysis of the mutant lesions may preferentially support one of these two explanations, and, in the latter case, identify specific functional subdomains within each protein.

What is the molecular nature of these genes that are required for the metaphase to anaphase transition during various types of cell divisions? Recent studies suggest that this checkpoint is functioning within one-cell C.

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Shakes, and A. Golden, manuscript in preparation , and Furuta et al. Although our results do not rule out the existence of such modifiers, they do indicate that such modifiers do not easily mutate to temperature sensitivity. Shakes, manuscript in preparation. Thus, something about either the function or molecular structure of the individual subunits must make them more or less likely to be isolated in such ts screens.

This possibility is supported by studies in S. Ts mutants proved critical to our analysis, since meiotic functions could not have been analyzed in nonconditional mutants with defects in germline proliferation.

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Additionally, screens for genetic suppressers may identify additional components that act in each of these pathways. Bowerman , the American Cancer Society to G. Seydoux, PF to D. Shakes , the Packard Foundation to G. Seydoux , the March of Dimes to G. Golden and P.