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A double-switch system regulates male courtship behavior in male and female Drosophila melanogaster.

Current models describe male-specific fruitless (fruM) as a genetic 'switch' regulating sexual behavior in Drosophila melanogaster, and they postulate that female (F) and male (M) doublesex (dsx) products control body sexual morphology. In contradiction to this simple model, we show that dsx, as well as fruM and non-sex-specific retained (retn), affect both male and female sexual behaviors. In females, both retn and dsxF contribute to female receptivity, and both genes act to repress male-like courtship activity in the presence or absence of fruM. In males, consistent with the opposing functions of dsxM and dsxF, dsxM acts as a positive factor for male courtship. retn also acts counter to fruM in the development of the male-specific muscle of Lawrence. Molecularly, retn seems to regulate sexual behavior via a previously described complex that represses zerknullt. Thus, we show that fru and dsx together act as a 'switch' system regulating behavior in the context of other developmental genes, such as retn.

Animals↗

Of microbes, mice and man.

This chapter reviews my 18 years of research in Anne's Unit including studies on temporal and spatial aspects of X-chromosome inactivation and imprinting and the role of methylation in X-inactivation in these processes during female mouse embryo development. To enable molecular studies of embryos, we developed a plethora of single cell assays for specific enzyme activity, gene mutation and methylation, and RNA transcription. While in Anne's Unit, I used these same single cell assays to pioneer the procedures for preimplantation diagnosis of genetic disease, now an established clinical approach to prevention of the birth of children with severe genetic disease. At the Institute of Child Health in London, we continue to develop new highly sensitive molecular procedures--currently for the creation of cDNA libraries from human preimplantation embryos, primordial germ cells and embryonal stem cells. We are using these cDNA preparations to isolate human developmental genes and embryo/cancer genes. One of the more fascinating aspects arising from my time in Anne's Unit is the way in which my research findings challenged a number of accepted dogmas in development concerned with the origin and totipotency of the germ line and the possibility of transgenerational genetic inheritance by epigenetic modification of the germ line.

Animals↗

Total tetra knockout of GP138 multigene family implicated in cell interactions in Dictyostelium discoideum.

The cellular slime mold Dictyostelium discoideum reproduces sexually under submerged and dark conditions. A cell surface glycoprotein gp138 has been identified as a target molecule for cell fusion-blocking antibodies, and is considered to be indispensable for the sexual cell fusion in this organism. Currently, four isoforms of gp138, DdFRP1alpha, DdFRP1beta, DdFRP2, and DdFRP3, are known. Genes encoding the latter three isoforms, GP138C, GP138A, and GP138B, have been isolated, comprising a GP138 multigene family. Here we isolated the fourth GP138 gene, GP138D, encoding DdFRP1alpha. These GP138 genes were found to cluster in a tandem array on chromosome 5, being bordered by two GP138-like sequences highly homologous to them but truncated. To clarify functional relationships among the GP138 family members, the entire GP138 region was deleted by a single knockout. Northern hybridization and western immuno-blotting analyses confirmed complete losses of GP138 mRNA and DdFRPs in the knockout strains, indicating that there are no more GP138 genes. Unexpectedly, however, the GP138-null mutants were fully potent for both sexual cell fusion and subsequent development. In addition, the original fusion-blocking antibodies detected a cell surface protein of close electrophoretic mobility to gp138 in the knockouts, suggesting the possibility that the actual target molecule of the fusion-blocking antibodies was not DdFRPs but this unidentified component. Since GP138-null mutants exhibited no obvious defects either in growth or asexual development, the real function of the GP138 family is unknown. Nevertheless, the expression levels of other developmental genes such as acaA, csaA, cotA-C, and spiA appeared to be altered in the GP138-null mutants. Therefore, it seems to have a non-critical but some role(s) during asexual development.

Amino Acid Sequence↗

Anecdotes, data and regulatory modules.

Beginning in the late 1980s, Eric Davidson's group at Cal Tech developed a modularity hypothesis of developmental gene regulation, showing that in an expanding number of cases, particular aspects of development were governed by compact 'modules' of transcription factor binding sites (TFBSs), and that these modules were separable, complex and interconnected. Davidson made no attempt to further generalize the hypothesis, but others took up the idea, transported it out of development and extended it to a general rule of clustering. Despite such misbegotten origins, the 'extended' modularity hypothesis--that TFBSs in general tend to come in compact clusters--has been highly productive, yet it has never been challenged with a large, diverse and unbiased dataset to see how universal it actually is. The aim of the present paper is to do so. Applying human-mouse-rat phylogenetic footprinting to neighbourhoods of a diverse set of TFBSs, including both developmental and non-developmental signals, we find that the extended hypothesis holds in at least 93.5% of cases. Based on this particular sample, we found a mean module length of 609 nucleotides containing, on an average, 24.5 presumptive regulatory signals of length greater than 5 and averaging 8.5 nucleotides each.

Animals↗

Deregulated expression of HOXB4 enhances the primitive growth activity of human hematopoietic cells.

Identification of the molecular mechanisms that can promote human hematopoietic stem cell amplification is a major goal in experimental and clinical hematology. Recent data indicate that a variety of regulatory molecules active in early development may also play a role in the maintenance of hematopoietic stem cells with repopulating activity. One important class of early developmental genes determining hematopoietic development are homeobox transcription factors. Here, we report that retrovirally mediated expression of the homeobox gene HOXB4 rapidly triggers an increase in the number of human hematopoietic cord blood cells with stem cell and progenitor cell properties detected both by in vitro and in vivo assays. This growth enhancement extended across primitive myeloid-erythroid and B-lymphoid progenitors but did not lead to alterations in the balance of lymphomyeloid reconstitution in vivo, suggesting that HOXB4 does not affect control of end-cell output. These findings reveal HOXB4 as a novel, positive regulator of the primitive growth activity of human hematopoietic progenitor cells and underline the relevance of early developmental factors for stem cell fate decisions.

Animals↗

2,3,7,8-Tetrachlorodibenzo-p-dioxin inhibits differentiation of normal diploid rat osteoblasts in vitro.

The influence of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), a potent halogenated aromatic hydrocarbon, on the development of bone tissue-like organization in primary cultures of normal diploid calvarial-derived rat osteoblasts was examined. Initially, when placed in culture, these cells actively proliferate while expressing genes associated with biosynthesis of the bone extracellular matrix. Then, post-proliferatively, genes are expressed that render the osteoblast competent for extracellular matrix mineralization and maintenance of structural as well as functional properties of the mature bone-cell phenotype. Our results indicate that, in the presence of TCDD, proliferation of osteoblasts was not inhibited but post-confluent formation of multicellular nodules that develop bone tissue-like organization was dramatically suppressed. Consistent with TCDD-mediated abrogation of bone nodule formation, expression of alkaline phosphatase and osteocalcin was not upregulated post-proliferatively. These findings are discussed within the context of TCDD effects on estrogens and vitamin D-responsive developmental gene expression during osteoblast differentiation and, from a broader biological perspective, on steroid hormone control of differentiation.

Animals↗

Delay in the fetal globin switch in infants of diabetic mothers.

In the normal fetus, a switch from production of hemoglobin F (alpha 2 gamma 2) to hemoglobin A (alpha 2 beta 2) occurs at 28 to 34 weeks of gestation. In the fetus with beta-hemoglobinopathy or beta-thalassemia, this switch proceeds despite the morbidity that results when production of beta-globin is abnormal or reduced. Since insulin has recently been shown to induce renewed expression of some inactive genes, we studied globin biosynthesis during the natural evolution of the fetal globin switch under conditions of hyperinsulinemia, which occurs in infants of diabetic mothers. Such infants develop in a hyperglycemic environment, which produces reactive hyperinsulinemia. The normal increase in beta-globin production from pre-switch levels did not occur in 9 of 10 such infants at term, as compared with 11 normal infants, in whom the switch occurred by 36 to 39 weeks of gestation (P less than 0.0001). The delay in the switch from gamma-globin to beta-globin in this unique clinical setting may allow identification of physiologic factors that can modulate developmental gene suppression.

Erythropoietin↗

Two promoters for the whiB sporulation gene of Streptomyces coelicolor A3(2) and their activities in relation to development.

Two transcripts corresponding to the whiB sporulation gene of Streptomyces coelicolor A3(2) that differed in length at their 5' ends by 164 nucleotides were identified by S1 mapping. Their presumptive promoters differed from each other; the more downstream, P2, resembled typical prokaryotic promoters (i.e., those recognized by the major form of RNA polymerase) at five of six positions in its -10 and -35 regions; and the more upstream, P1, was comparably similar, instead, to the previously described hrdDp1 promoter (M. J. Buttner, K. F. Chater, and M. J. Bibb, J. Bacteriol. 172:3367-3378, 1990) around -40, -10, and +1. In surface cultures of the wild-type strain, the abundance of transcripts from the weak P1 promoter showed no obvious correlation with the developmental stage, whereas transcripts from P2 were barely detectable until aerial mycelium was present and then became relatively abundant, consistent with the developmental role of whiB. Both types of transcript were detected during and, to a lesser extent, after rapid growth in liquid culture. In addition, both promoters were utilized in vitro by RNA polymerase purified from a liquid culture of S. coelicolor. Transcription from P1 and P2 was observed during surface culture in strains carrying mutations blocking aerial mycelium formation (bldA and bldB) or the formation of spores in aerial mycelium (whiA, whiB, whiG, and whiH). Thus, whiB transcription is not severely dependent on any of these developmental genes, among which whiG is the determinant of a putative sigma factor specific for, and crucial to, sporulation.

Base Sequence↗

MAP kinase and cAMP filamentation signaling pathways converge on the unusually large promoter of the yeast FLO11 gene.

In Saccharomyces cerevisiae, two major signal transduction pathways, the Kss1 MAPK pathway and the cAMP-regulated pathway, are critical for the differentiation of round yeast form cells to multicellular, invasive pseudohyphae. Here we report that these parallel pathways converge on the promoter of a gene, FLO11, which encodes a cell surface protein required for pseudohyphal formation. The FLO11 promoter is unusually large, containing at least four upstream activation sequences (UASs) and nine repression elements which together span at least 2.8 kb. Several lines of evidence indicate that the MAPK and cAMP signals are received by distinct transcription factors and promoter elements. First, regulation via the MAPK pathway requires the transcription factors Ste12p/Tec1p, whereas cAMP-mediated activation requires a distinct factor, Flo8p. Secondly, mutations in either pathway block FLO11 transcription. Overexpression of STE12 can suppress the loss of FLO8, and overexpression of FLO8 can suppress the loss of STE12. Finally, multiple distinct promoter regions of the FLO11 promoter are required for its activation by either Flo8p or Ste12p/ Tec1p. Thus, like the promoters of the key developmental genes, HO and IME1, the FLO11 promoter is large and complex, endowing it with the ability to integrate multiple inputs.

Calcium-Calmodulin-Dependent Protein Kinases↗

Branched-chain fatty acids: the case for a novel form of cell-cell signalling during Myxococcus xanthus development.

The esg locus is required for the formation of multicellular fruiting bodies and spores by the developmental bacterium Myxococcus xanthus. Studies have suggested that esg mutants are defective in the production of an essential signal (E-signal) used in cell-cell communication and that E-signalling is required for the expression of many developmental genes. Recently we have determined that the esg locus encodes components of a branched-chain keto acid dehydrogenase, a multienzyme complex involved in branched-chain amino acid metabolism in many bacteria and higher organisms. During vegetative growth in M. xanthus, this enzyme complex appears to participate in the production of the branched-chain fatty acids found in this organism. M. xanthus fatty acids (including the branched-chain fatty acids) have been observed to have a variety of effects on developing cells. These effects include: (i) the lysis of M. xanthus cells (autocide activity), (ii) acceleration of the rate of sporulation and (iii) rescue of sporulation by certain development-defective mutants. These and other results suggest a model in which the branched-chain fatty acids, synthesized during growth, are released from cellular phospholipid by a developmentally regulated phospholipase during fruiting-body formation. This model proposes that one or more of the branched-chain fatty acids that are released constitutes the E-signal which must be transmitted between cells to complete M. xanthus development.

Amino Acids, Branched-Chain↗

Localisation of X linked recessive idiopathic hypoparathyroidism to a 1.5 Mb region on Xq26-q27.

X linked recessive idiopathic hypoparathyroidism (HPT) has been observed in two kindreds from Missouri, USA. Affected subjects, who are males, suffer from infantile onset of epilepsy and hypocalcaemia, which appears to be the result of an isolated congenital defect of parathyroid gland development; females are not affected and are normocalcaemic. The gene causing HPT has been previously mapped to a 7 cM interval, flanked centromerically by F9 and telomerically by DXS98, in Xq26-q27, and an analysis of mitochondrial DNA has established a common ancestry for these two kindreds. In order to define further the map location of HPT and thereby facilitate its isolation, we have undertaken linkage studies using polymorphic loci whose order has been established as Xcen - DXS1001 - DXS294 - DXS102 - F9 - DXS1232 - DXS984 - CDR1 - DXS105 - DXS1205 - DXS1227 - DXS98 - DXS52 - Xqter, within this region. Our results established linkage (lod score > 3) between HPT and eight of these 12 loci and indicated that the most likely location of HPT was within a 1.5 Mb interval flanked centromerically by F9 and telomerically by DXS984. Thus, the results of this study have helped to refine the map location of HPT, and this will facilitate the identification of this putative developmental gene and its role in the embryological formation of the parathyroids.

Chromosome Mapping↗

Starting from fins: parallelism in the evolution of limbs and genitalia: the fin-to-genitalia transition.

Organizers of the symposium Starting from Fins: Parallelism in the Evolution of Limbs and Genitalia intended it 1) to begin debates and discussions about parallelism, serial homology and transitions in development, as well as evolution of gene function and theories of origins and 2) to examine closely the potential significance of serial homology in understanding the evolution of morphology. This issue of Evolution and Development focuses on unpaired fin to genitalia transitions; the July-August issue will focus on paired fins to limbs, revisit the issues raised in the symposium, and point to future directions. Minelli's opening presentation introduced the central theme of the symposium by suggesting that body appendages such as arthropod and vertebrate limbs, chordate tails and external genitalia are evolutionarily divergent duplicates (paramorphs) of the main body axis. Suzuki's and Podlasek's presentations focused on the development of mammalian genitalia. Suzuki presented Suzuki et al investigations of the role of fibroblast growth factor (Fgf) and Sonic hedgehog (Shh) as signaling molecules during murine external genitalia formation, and Podlasek presented Podlasek et al investigations to elucidate a rudimentary pathway of essential developmental genes and transcriptional regulators such as Hox genes, Sonic hedgehog (Shh), and Bone morphogenetic proteins 2 and 4 (BMP-2; BMP-4), found in the limb. Discussions and questions emerging from the symposium point to the need to recognize that claims of phylogenetic cause must be based on something more than similarities; research must focus on the extent to which comparisons can be taken as well as on the evolutionary significance of similarities.

Animals↗

An expressed sequence tag (EST) library from developing fruits of an Hawaiian endemic mint (Stenogyne rugosa, Lamiaceae): characterization and microsatellite markers.

BACKGROUND: The endemic Hawaiian mints represent a major island radiation that likely originated from hybridization between two North American polyploid lineages. In contrast with the extensive morphological and ecological diversity among taxa, ribosomal DNA sequence variation has been found to be remarkably low. In the past few years, expressed sequence tag (EST) projects on plant species have generated a vast amount of publicly available sequence data that can be mined for simple sequence repeats (SSRs). However, these EST projects have largely focused on crop or otherwise economically important plants, and so far only few studies have been published on the use of intragenic SSRs in natural plant populations. We constructed an EST library from developing fleshy nutlets of Stenogyne rugosa principally to identify genetic markers for the Hawaiian endemic mints. RESULTS: The Stenogyne fruit EST library consisted of 628 unique transcripts derived from 942 high quality ESTs, with 68% of unigenes matching Arabidopsis genes. Relative frequencies of Gene Ontology functional categories were broadly representative of the Arabidopsis proteome. Many unigenes were identified as putative homologs of genes that are active during plant reproductive development. A comparison between unigenes from Stenogyne and tomato (both asterid angiosperms) revealed many homologs that may be relevant for fruit development. Among the 628 unigenes, a total of 44 potentially useful microsatellite loci were predicted. Several of these were successfully tested for cross-transferability to other Hawaiian mint species, and at least five of these demonstrated interesting patterns of polymorphism across a large sample of Hawaiian mints as well as close North American relatives in the genus Stachys. CONCLUSION: Analysis of this relatively small EST library illustrated a broad GO functional representation. Many unigenes could be annotated to involvement in reproductive development. Furthermore, first tests of microsatellite primer pairs have proven promising for the use of Stenogyne rugosa EST SSRs for evolutionary and phylogeographic studies of the Hawaiian endemic mints and their close relatives. Given that allelic repeat length variation in developmental genes of other organisms has been linked with morphological evolution, these SSRs may also prove useful for analyses of phenotypic differences among Hawaiian mints.

5' Untranslated Regions↗

Interdigitated deletion complexes on mouse chromosome 5 induced by irradiation of embryonic stem cells.

Chromosome deletions have several applications in the genetic analysis of complex organisms. They can be used as reagents in region-directed mutagenesis, for mapping of simple or complex traits, or to identify biological consequences of segmental haploidy, the latter being relevant to human contiguous gene syndromes and imprinting. We have generated three deletion complexes in ES (Embryonic Stem) cells that collectively span approximately 40 cM of proximal mouse chromosome 5. The deletion complexes were produced by irradiation of F(1) hybrid ES cells containing herpes simplex virus thymidine kinase genes (tk) integrated at the Dpp6, Hdh (Huntington disease locus), or Gabrb1 loci, followed by selection for tk-deficient clones. Deletions centered at the adjacent Hdh and Dpp6 loci ranged up to approximately 20 cM or more in length and overlapped in an interdigitated fashion. However, the interval between Hdh and Gabrb1 appeared to contain a locus haploinsufficient for ES cell viability, thereby preventing deletions of either complex from overlapping. In some cases, the deletions resolved the order of markers that were previously genetically inseparable. A subset of the ES cell-bearing deletions was injected into blastocysts to generate germline chimeras and establish lines of mice segregating the deletion chromosomes. At least 11 of the 26 lines injected were capable of producing germline chimeras. In general, those that failed to undergo germline transmission bore deletions larger than the germline-competent clones, suggesting that certain regions of chromosome 5 contain haploinsufficient developmental genes, and/or that overall embryonic viability is cumulatively decreased as more genes are rendered hemizygous. Mice bearing deletions presumably spanning the semidominant hammertoe locus (Hm) had no phenotype, suggesting that the classic allele is a dominant, gain-of-function mutation. Overlapping deletion complexes generated in the fashion described in this report will be useful as multipurpose genetic tools and in systematic functional mapping of the mouse genome.

Animals↗

Human homologue of cement gland protein, a novel metastasis inducer associated with breast carcinomas.

A suppression subtractive cDNA library representing mRNAs expressed at a higher level in the malignant human breast cancer cell line, MCF-7, relative to a benign breast tumor-derived cell line, Huma 123, contained a cDNA, M36, which was expressed in estrogen receptor alpha (ERalpha)-positive breast carcinoma cell lines but not in cell lines from normal/benign/ERalpha-negative malignant breast lesions. M36 cDNA had an identical coding sequence to anterior gradient 2 (AGR2), the human homologue of the cement gland-specific gene (Xenopus laevis). Screening of breast tumor specimens using reverse transcription-PCR and immunocytochemistry with affinity-purified anti-AGR2 antibodies showed that the presence of AGR2 mRNA and protein were both statistically significantly associated with ERalpha-positive carcinomas (P = 0.007, Fisher's exact test) and with malignancy (P < or = 0.025). When an expression vector for AGR2 cDNA was introduced into benign nonmetastatic rat mammary tumor cells, and three separate clones and two pools of cells were transferred to the mammary glands of syngeneic hosts, there were no consistent differences in the mean latent periods of tumor formation. However, metastases occurred in the lungs of animals receiving the AGR2 transfectants in 77% to 92% of animals with primary tumors (P = 0.0001) compared with no metastases in the control groups. The AGR2 transfectants exhibited enhanced rates of adhesion to a plastic substratum and extracellular AGR2 enhanced the rate of attachment of AGR2-negative but not AGR2-positive cells. These experiments are the first to link mechanistically the developmental gene product, AGR2, with metastasis in vivo.

Animals↗

Functional PAX-6 gene-linked polymorphic region: potential association with paranoid schizophrenia.

BACKGROUND: Early differentiation of the nervous system and adult CNS neuroplasticity is modulated by PAX-6. We have shown previously that a highly polymorphic, functional AC/AG repeat in the 5' regulatory region of the gene showed significantly increased promoter activity, if containing > or = 29 repeats, and that the heterozygous genotype (< or = 28/> or = 29) revealed increased mRNA PAX-6 levels in human brain tissue compared to the homozygous short variant. METHODS: In a case-control study of 655 unrelated individuals, allele frequencies and genotype distributions of the functional PAX-6 promoter polymorphism were investigated comprising patients with DSM-IV schizophrenia, patients with affective disorders, and population controls. RESULTS: No allelic or genotypic association of the PAX-6 promoter polymorphism to affective disorder or to schizophrenia as one disease entity was observed. After subtyping schizophrenia into paranoid and nonparanoid forms, potential evidence was found for a genotypic association of the high-activity variant with the paranoid subtype of schizophrenia (p = .02). The estimated odds ratio was 1.7 (95% CI .98 to 2.95) for those heterozygous and 1.4 (95% CI .82 to 2.42) for those heterozygous or homozygous for the high-activity variant compared to the homozygous low-activity variant. CONCLUSIONS: Our finding indicates that early developmental genes may be involved in the etiopathogenesis of schizophrenia subtypes via variable transcriptional regulation in the developing and adult human brain.

Adult↗

Metazoan Scc4 homologs link sister chromatid cohesion to cell and axon migration guidance.

Saccharomyces cerevisiae Scc2 binds Scc4 to form an essential complex that loads cohesin onto chromosomes. The prevalence of Scc2 orthologs in eukaryotes emphasizes a conserved role in regulating sister chromatid cohesion, but homologs of Scc4 have not hitherto been identified outside certain fungi. Some metazoan orthologs of Scc2 were initially identified as developmental gene regulators, such as Drosophila Nipped-B, a regulator of cut and Ultrabithorax, and delangin, a protein mutant in Cornelia de Lange syndrome. We show that delangin and Nipped-B bind previously unstudied human and fly orthologs of Caenorhabditis elegans MAU-2, a non-axis-specific guidance factor for migrating cells and axons. PSI-BLAST shows that Scc4 is evolutionarily related to metazoan MAU-2 sequences, with the greatest homology evident in a short N-terminal domain, and protein-protein interaction studies map the site of interaction between delangin and human MAU-2 to the N-terminal regions of both proteins. Short interfering RNA knockdown of human MAU-2 in HeLa cells resulted in precocious sister chromatid separation and in impaired loading of cohesin onto chromatin, indicating that it is functionally related to Scc4, and RNAi analyses show that MAU-2 regulates chromosome segregation in C. elegans embryos. Using antisense morpholino oligonucleotides to knock down Xenopus tropicalis delangin or MAU-2 in early embryos produced similar patterns of retarded growth and developmental defects. Our data show that sister chromatid cohesion in metazoans involves the formation of a complex similar to the Scc2-Scc4 interaction in the budding yeast. The very high degree of sequence conservation between Scc4 homologs in complex metazoans is consistent with increased selection pressure to conserve additional essential functions, such as regulation of cell and axon migration during development.

Animals↗

Developmental regulation of SPO13, a gene required for separation of homologous chromosomes at meiosis I.

Previous studies have demonstrated that the SPO13 gene is required for chromosome separation during meiosis I in Saccharomyces cerevisiae. In the presence of the spo13-1 nonsense mutation, MATa/MAT alpha diploid cells complete a number of events typical of meiosis I including premeiotic DNA synthesis, genetic recombination, and spindle formation. Disjunction of homologous chromosomes, however, fails to occur. Instead, cells proceed through a single meiosis II-like division and form two diploid spores. In this paper, we report the cloning of this essential meiotic gene and an analysis of its transcription during vegetative growth and sporulation. Disruptions of SPO13 in haploid and diploid cells show that it is dispensible for mitotic cell division. Diploids homozygous for the disruptions behave similarly to spo13-1 mutants; they sporulate at wild-type levels and produce two-spored asci. The DNA region complementing spo13-1 encodes two overlapping transcripts, which have the same 3' end but different 5' ends. The major transcript is 400 bases shorter than the larger, less abundant one. The shorter RNA is sufficient to complement the spo13-1 mutation. While both transcripts are undetectable or just barely detectable in vegetative cultures, they each undergo a greater than 70-fold induction early during sporulation, reaching a maximum level about the time of the first meiotic division. In synchronously sporulating populations, the transcripts nearly disappear before the completion of ascus formation. Nonsporulating cells homozygous for the mating-type locus show a small increase in abundance (less than 5% of the increase in sporulating cells) of both transcripts in sporulation medium. These results indicate that expression of the SPO13 gene is developmentally regulated and starvation alone, independent of the genotype at MAT, can trigger initial induction.

Chromosomes↗