Failure Of Meiosis Research Articles

Bouquet Formation Failure in Meiosis of F1 Wheat-Rye Hybrids with Mitotic-Like Division.

Bouquet formation is believed to be involved in initiating homologous chromosome pairings in meiosis. A bouquet is also formed in the absence of chromosome pairing, such as in F1 wheat–rye hybrids. In some hybrids, meiosis is characterized by a single, mitotic-like division that leads to the formation of unreduced gametes. In this study, FISH with the telomere and centromere-specific probe, and immunoFISH with ASY1, CENH3 and rye subtelomere repeat pSc200 were employed to perform a comparative analysis of early meiotic prophase nuclei in four combinations of wheat–rye hybrids. One of these, with disomic rye chromosome 2R, is known to undergo normal meiosis, and here, 78.9% of the meiocytes formed a normal-appearing telomere bouquet and rye subtelomeres clustered in 83.2% of the meiocytes. In three combinations with disomic rye chromosomes 1R, 5R and 6R, known to undergo a single division of meiosis, telomeres clustered in 11.4%, 44.8% and 27.6% of the meiocytes, respectively. In hybrids with chromosome 1R, rye subtelomeres clustered in 12.19% of the meiocytes. In the remaining meiocytes, telomeres and subtelomeres were scattered along the nucleus circumference, forming large and small groups. We conclude that in wheat–rye hybrids with mitotic-like meiosis, chromosome behavior is altered already in the early prophase.

12. Cancer cytogenomic array analysis reveals origin of ovarian teratoma and reproductive lessons learned from it

Ovarian teratoma may be derived from germ cells at any developmental stage from premeiotic oogonia through meiotic oocytes to mature, post-meiotic ova. We analyzed fresh tissue samples from 27 primary ovarian teratomas and 3 extragonadal deposits (age: 4-16 years) using CytoScan array and karyotype. Array analysis detected five patterns of copy neutral loss of heterozygosity (CN-LOH). Failure of meiosis I (Type I error) with CN-LOH in the p arm and/or q arm of chromosomes without spanning centromeres was observed in 13 cases, Type II error characterized by homozygosity spanning centromeres in 6 cases, Type III error with homozygosity of the entire genome via endoreduplication of a haploid ovum in 3 cases, Type IV error with no acquired CN-LOH in 4 cases, and Type V error with both meiotic I and meiotic II non-disjunction in 1 case.

Effects of Environmental and Pathological Hypoxia on Male Fertility.

Male infertility is a widespread health problem affecting approximately 6%–8% of the male population, and hypoxia may be a causative factor. In mammals, two types of hypoxia are known, including environmental and pathological hypoxia. Studies looking at the effects of hypoxia on male infertility have linked both types of hypoxia to poor sperm quality and pregnancy outcomes. Hypoxia damages testicular seminiferous tubule directly, leading to the disorder of seminiferous epithelium and shedding of spermatogenic cells. Hypoxia can also disrupt the balance between oxidative phosphorylation and glycolysis of spermatogenic cells, resulting in impaired self-renewal and differentiation of spermatogonia, and failure of meiosis. In addition, hypoxia disrupts the secretion of reproductive hormones, causing spermatogenic arrest and erectile dysfunction. The possible mechanisms involved in hypoxia on male reproductive toxicity mainly include excessive ROS mediated oxidative stress, HIF-1α mediated germ cell apoptosis and proliferation inhibition, systematic inflammation and epigenetic changes. In this review, we discuss the correlations between hypoxia and male infertility based on epidemiological, clinical and animal studies and enumerate the hypoxic factors causing male infertility in detail. Demonstration of the causal association between hypoxia and male infertility will provide more options for the treatment of male infertility

Mathematical Modeling and Sensitivity Analysis of the Existence of Male Calico Cats Population Based on Cross Breeding of All Coat Colour Types

The coat color of cats is normally governed by genes found on the X chromosome in both male chromosome XY and female chromosome XX. The meiosis failure in the process of gametogenesis leads to the birth of three-colored male cats caused by an excess of the X chromosome in the male chromosome type XY. The chromosome structure of three-color male cats, called male calico cats, appeared similar to the XXY Klinefelter’s syndrome in human. Mathematical modeling and investigation of the factors that influence the infrequency of male calico cats are our main objectives of this paper. In addition, we also discuss the possible contributions and strategies to overcome the scarcity of these cats. We construct a mathematical model based on a combination of genes in the chromosome that regulates the color of cat coat on the fertilization process. The mathematical model is given as a six-dimensional system of differential equations. Sensitivity analysis is used to investigate the important parameters in the existence of male calico cats. Our finding states that the probability of normal male cats meiosis is a crucial parameter in the maintenance of the existence of male calico cats. Furthermore, one of the strategies that we could recommend in maintaining the existence of male calico cats is minimizing the value of the successful meiosis probability of normal male cats.

The MAP3K-Coding QUI-GON JINN (QGJ) Gene Is Essential to the Formation of Unreduced Embryo Sacs in Paspalum.

Apomixis is a clonal mode of reproduction via seeds, which results from the failure of meiosis and fertilization in the sexual female reproductive pathway. In previous transcriptomic surveys, we identified a mitogen-activated protein kinase kinase kinase (N46) displaying differential representation in florets of sexual and apomictic Paspalum notatum genotypes. Here, we retrieved and characterized the N46 full cDNA sequence from sexual and apomictic floral transcriptomes. Phylogenetic analyses showed that N46 was a member of the YODA family, which was re-named QUI-GON JINN (QGJ). Differential expression in florets of sexual and apomictic plants was confirmed by qPCR. In situ hybridization experiments revealed expression in the nucellus of aposporous plants’ ovules, which was absent in sexual plants. RNAi inhibition of QGJ expression in two apomictic genotypes resulted in significantly reduced rates of aposporous embryo sac formation, with respect to the level detected in wild type aposporous plants and transformation controls. The QGJ locus segregated independently of apospory. However, a probe derived from a related long non-coding RNA sequence (PN_LNC_QGJ) revealed RFLP bands cosegregating with the Paspalum apospory-controlling region (ACR). PN_LNC_QGJ is expressed in florets of apomictic plants only. Our results indicate that the activity of QGJ in the nucellus of apomictic plants is necessary to form non-reduced embryo sacs and that a long non-coding sequence with regulatory potential is similar to sequences located within the ACR.

Transcriptome analysis reveals new microRNAs-mediated pathway involved in anther development in male sterile wheat

Background337S is a novel bi-pole-photo-thermo-sensitive genic male sterile line in wheat, and sensitive to both long day length/high temperature and short day length/low temperature condition. Although the regulatory function of MicroRNAs (miRNAs) in reproductive development has been increasingly studied, their roles in pre-meiotic and meiotic cells formation of plants have not been clearly explored. Here, we explored the roles of miRNAs in regulating male sterility of 337S at short day length/low temperature condition.ResultsSmall RNA sequencing and degradome analyses were employed to identify miRNAs and their targets in the 337S whose meiotic cells collapsed rapidly during male meiotic prophase, resulting in failure of meiosis at SL condition. A total of 102 unique miRNAs were detected. Noticeably, the largest miRNA family was MiR1122. The target CCR4-associated factor 1 (CAF1) of miR2275, a subunit of the Carbon Catabolite Repressed 4-Negative on TATA-less (CCR4-NOT) complex, contributes to the process of early meiosis, and was first identified here. Further studies showed that the expression of several pivotal anther-related miRNAs was altered in 337S at SL condition, especially tae-miR1127a, which may be related to male sterility of 337S. Here, we also identified a new member of SWI/SNF factors SWI/SNF-related matrix-associated actin-dependent regulator of chromatin subfamily A, member 3-like 3 (SMARCA3L3) targeted by tae-miR1127a, whose function might be involved in faithful progression of meiosis in male reproductive cells.ConclusionThe miRNA-target interactions of tae-miR2275-CAF1 and tae-miR1127a-SMARCA3L3 might be involved in regulating male fertility in 337S. Our results also implied that multiple roles for SMARCA3L3 and CAF1 in DNA repair and transcriptional regulation jointly orchestrated a tight and orderly system for maintaining chromatin and genome integrity during meiosis.

Recurrent triploid digynic conceptions and mature ovarian teratomas: Are they different manifestations of the same genetic defect?

Miscarriages affect 15% of clinically recognized pregnancies. Recurrent miscarriage (RM) is defined by the occurrence of at least two consecutive pregnancy losses and affects 1%-5% of couples trying to conceive. In an attempt to categorize patients with RM and identify the mechanisms leading to their miscarriages, we first used flow cytometry to assess the ploidy of 93 products of conception (POCs) from 53 patients with RM (≥3 miscarriages). We identified a single patient with four triploid POCs. We then used fluorescent in situ hybridization to confirm the triploidies and fluorescent microsatellite genotyping with distal and pericentromeric markers to determine their parental origin and the mechanisms leading to their formation. We found that all four triploidies were digynic and due to a failure in meiosis II (MII), suggesting a genetic predisposition. Upon further investigation into the family, we found a remarkable history of ovarian cysts and dysfunctions on the maternal side. Notably, one maternal cousin had a mature ovarian teratoma that we analyzed and found an identical mechanism at its origin, a failure in MII. The identification of two patients in the same family with two different manifestations-digynic triploid conceptions and mature ovarian teratomas, both resulting from the failure of MII-suggests an inherited genetic susceptibility toward an error in MII segregating in the family that may manifest in the form of a triploid digynic miscarriage or a mature ovarian teratoma. Our findings may facilitate the future identification of causative mutations for MII defects.

Evidence of metachronous development of ovarian teratomas: a case report of bilateral mature cystic teratomas of the ovaries and systematic literature review

BackgroundMature cystic teratomas are usually found in the ovaries. They are bilateral in 10 to 15% of cases and multiple cystic teratomas may be present in one ovary. The aim of this study is to clarify if development of mature cystic teratomas of the ovaries in a single host is metachronous or due to autoimplant or recurrence.Case presentationWe report a woman with bilateral mature cystic teratomas of the ovaries. DNA profiles of these teratomas were investigated via short tandem repeat (STR) analysis and methylation statuses were determined via methylation sensitive multiplex ligation-dependent probe amplification methods. The results showed that the cystic teratomas originated from different stages of oogonia or primary oocyte before germinal vesicle stage failure of meiosis I in female gametogenesis.Potentially relevant literature was searched in PubMed database. Cases of bilateral or multiple mature cystic teratomas of the ovaries were analyzed. To date, there has been no reported case of multiple mature cystic teratomas in which clarification of the origin was achieved using molecular genetic methods.ConclusionsThe results of this case study provide evidence of metachronous development of mature cystic teratomas of the ovaries and may serve as a reference in the management of patients following laparoscopic cystectomy.

Loss of protein phosphatase 6 in oocytes causes failure of meiosis II exit and impaired female fertility

Dynamic protein phosphorylation and dephosphorylation, mediated by a conserved cohort of protein kinases and phosphatases, regulate cell cycle progression. Among the well-known PP2A-like protein phosphatases, protein phosphatase 6 (PP6) has been analyzed in mammalian mitosis, and Aurora A has recently been identified as its key substrate. However, the functions of PP6 in meiosis are still entirely unknown. To identify the physiological role of PP6 in female gametogenesis, Ppp6c(F/F) mice were first generated and crossed with Zp3-Cre mice to selectively disrupt Ppp6c expression in oocytes. Here, we report for the first time that PP6c is dispensable for oocyte meiotic maturation but essential for exit from meiosis II (MII) after fertilization. Depletion of PP6c caused an abnormal MII spindle and disrupted MII cytokinesis, resulting in zygotes with high risk of aneuploidy and defective early embryonic development, and thus severe subfertility. We also reveal that PP6 inactivation interferes with MII spindle formation and MII exit owing to increased Aurora A activity, and that Aurora A inhibition with MLN8237 can rescue the PP6c depletion phenotype. In conclusion, our findings uncover a hitherto unknown role for PP6 as an indispensable regulator of oocyte meiosis and female fertility.

Construct of RNAi plasmids and Their Application For the Study of Meiotic Proteins Through RNA Interference

Sexual reproduction in eukaryotes requires production of haploid gametes from diploid cells. This is accomplished through meiosis, in which two successive divisions of a diploid cell in the germ line results in four haploid gametes. This process is highly regulated, and requires the action of many key proteins in order for chromosomes to segregate properly and meiosis to be successful. In the absence of a protein involved in meiosis, one may expect chromosome missegregation, failure of meiosis, and eventual cell apoptosis. In this study, the function of meiotic proteins are analyzed through the process of RNA interference in Caenorhabditis elegans, a model organism for the study of meiosis. RNA interference (RNAi) reversibly modifies the expression of proteins due to the introduction of double‐stranded RNA (dsRNA), which results in the reversible depletion, or silencing, of the protein encoded by the complementary gene. In previous work, we used proteomics to identify candidate meiosis proteins. In order to evaluate these candidates, we constructed RNAi plasmids that would target the gene under investigation. A successful RNAi construct will result in the decreased expression of the target protein. If the protein is required for proper completion of meiosis, the process will be disrupted, resulting in the reduction in viability of C. elegans progeny. This poster will present data on the construct of RNAi plasmids and their subsequent effects on meiosis in C. elegans, as well as direct analysis of the cytology of meiosis through fluorescence microscopy.

MEIOB exhibits single-stranded DNA-binding and exonuclease activities and is essential for meiotic recombination

Meiotic recombination enables the reciprocal exchange of genetic material between parental homologous chromosomes and ensures faithful chromosome segregation during meiosis in sexually reproducing organisms. This process relies on the complex interaction of DNA repair factors, and many steps remain poorly understood in mammals. Here we report the identification of MEIOB, a meiosis-specific protein, in a proteomics screen for novel meiotic chromatin-associated proteins in mice. MEIOB contains an OB domain with homology to one of the RPA1 OB folds. MEIOB binds to single-stranded DNA and exhibits 3’ to 5’ exonuclease activity. MEIOB forms a complex with RPA and with SPATA22, and these three proteins colocalize in foci that are associated with meiotic chromosomes. Strikingly, chromatin localization and stability of MEIOB depends on SPATA22 and vice versa. Meiob-null mouse mutant exhibits a failure in meiosis and sterility in both sexes. Our results suggest that MEIOB is required for meiotic recombination and chromosomal synapsis.

Meiosis arrest female 1 (MARF1) has nuage-like function in mammalian oocytes

Orderly regulation of meiosis and protection of germline genomic integrity from transposable elements are essential for male and female gamete development. In the male germline, these processes are ensured by proteins associated with cytoplasmic nuage, but morphologically similar germ granules or nuage have not been identified in mammalian female germ cells. Indeed, many mutations affecting nuage-associated proteins such as PIWI and tudor domain containing proteins 5 and 7 (TDRD5/7) can result in failure of meiosis, up-regulation of retrotransposons, and infertility only in males and not in females. We recently identified MARF1 (meiosis arrest female 1) as a protein essential for controlling meiosis and retrotransposon surveillance in oocytes; and in contrast to PIWI-pathway mutations, Marf1 mutant females are infertile, whereas mutant males are fertile. Here we put forward the hypothesis that MARF1 in mouse oocytes is a functional counterpart of the nuage-associated components of spermatocytes. We describe the developmental pattern of Marf1 expression and its roles in retrotransposon silencing and protection from DNA double-strand breaks. Analysis of MARF1 protein domains compared with PIWI and TDRD5/7 revealed that these functional similarities are reflected in remarkable structural analogies. Thus, functions that in the male germline require protein interactions and cooperative scaffolding are combined in MARF1, allowing a single molecule to execute crucial activities of meiotic regulation and protection of germline genomic integrity.

Non-muscle myosin IIB is essential for cytokinesis during male meiotic cell divisions

Cytokinesis, the final stage of cell division, bisects the cytoplasm into two daughter cells. In mitotic cells, this process depends on the activity of non-muscle myosin II (NMII), a family of actin-binding motor-proteins that participate in the formation of the cleavage furrow. The relevance of NMII for meiotic cell division, however, is poorly understood. The NMII family consists of three members, NMIIA, NMIIB, and NMIIC, containing different myosin heavy chains (MYH9, MYH10, and MYH14, respectively). We find that a single non-muscle myosin II, NMIIB, is required for meiotic cytokinesis in male but not female mice. Specifically, NMIIB-deficient spermatocytes exhibit cytokinetic failure in meiosis I, resulting in bi-nucleated secondary spermatocytes. Additionally, cytokinetic failure at meiosis II gives rise to bi-nucleated or even tetra-nucleated spermatids. These multi-nucleated spermatids fail to undergo normal differentiation, leading to male infertility. In spite of the presence of multiple non-muscle myosin II isoforms, we demonstrate that a single member, NMIIB, plays an essential and non-redundant role in cytokinesis during meiotic cell divisions of the male germline.

Expression Analysis of MLH3, MLH1, and MSH4 in Maturation Arrest

The expression of DNA mismatch repair (DMMR) genes in patients with maturation arrest (MA) was analyzed. Samples were subjected to mutL homolog 3 (MLH3) mutation analysis by denaturing high-performance liquid chromatography/sequencing and quantification of MMR expression in testicular tissue by real-time polymerase chain reaction (PCR). Microsatellite instability assays were negative. Two missense and 1 intronic mutations were found. The missense mutation 2531C/T (P844L), predicted to affect MLH3 function, was found in 3 MA cases in association with the intronic variant IVS9 + 66G/A. Relative messenger RNA (mRNA) quantification identified 2 patients who overexpressed MLH3, 1 of them also overexpressing mutL homolog 1 (MLH1). The latter also presented the 2531C/T-IVS9 + 66G/A mutation. In conclusion, we suggest that a predominance of MLH3 expression might favor the MLH1/MLH3 complex which then would compete with the MLH1/PMS2 complexes. This could convey disruption of the relative stoichiometry between MLH1/MLH3 and MLH1/PMS2 complexes, thus causing meiosis failure, as MLH1/PMS2 complexes are supposed to replace MLH1/MLH3 during diplonema.

Two types of partial fertility in a diploid population of the fern Thelypteris decursive-pinnata (Thelypteridaceae)

Two types of abnormal sporophytes were observed in a population of diploid Thelypteris decursive-pinnata. Most sporophytes in this population exhibited regular chromosome pairing, resulting in the formation of 30 bivalents in meiosis I; however, they produced abortive spores to various degrees. Some formed large globose spores at low frequencies, most likely to be unreduced diplospores. The other type of abnormal sporophyte underwent synaptic failure to form 60 univalents at meiosis I, but produced fertile spores, mostly large globose ones at low frequencies. The globose spores were considered unreduced diplospores because the gametophytes arising from them produced tetraploid sporophytes by gametophytic selfing. One tetraploid formed only univalents at meiosis I. Allozyme variation was not detected in this population, although neighboring ordinary diploid populations exhibited it to a certain degree. The sympatric occurrence and allozyme uniformity of the two groups suggest that both are offspring of a founder sporophyte, which may have possessed two types of mutated recessive genes responsible for the spore sterility and the synaptic failure in meiosis. Unreduced spores formed by these two types may play an important role in the polyploid speciation of this species.

Semen quality in men with Y chromosome aberrations

Infertile males sometimes bear structurally balanced chromosome aberrations, such as translocations and inversions, which involve both autosomes and sex chromosomes. The aim of this study was to evaluate genotype-phenotype correlations in a sample of infertile men with various types of Y chromosome abnormalities. In particular, we examined the effect of (i) balanced structural aberrations such as translocations between sex chromosomes and autosomes; (ii) unbalanced structural aberrations such as deletions or isodicentrics, both [idic(Yp)] and [idic(Yq)]. We studied 13 subjects bearing Y chromosome aberrations. Each patient underwent seminal fluid examination, andrological inspection, hormone study, testicular ultrasound, conventional and molecular cytogenetic analysis and study of Y chromosome microdeletions. Comparison of genotype and sperm phenotype in infertile patients with various Y chromosome aberrations revealed the key role of meiotic pairing defects in arresting spermatogenesis, both in the presence and in the absence of azoospermic factor microdeletions and cell mosaicism. The failure of meiosis and, in consequence, spermatogenesis may be a result of the failure to inactivate the X chromosome in the meiotic prophase, which is necessary for normal male spermatogenesis to take place.

Aurora-C Kinase Deficiency Causes Cytokinesis Failure in Meiosis I and Production of Large Polyploid Oocytes in Mice

We previously isolated Aurora-C/Aie1 in a screen for kinases expressed in mouse sperm and eggs. Here, we show the localization of endogenous Aurora-C and examine its roles during female mouse meiosis. Aurora-C was detected at the centromeres and along the chromosome arms in prometaphase I-metaphase I and was concentrated at centromeres at metaphase II, in which Aurora-C also was phosphorylated at Thr171. During the anaphase I-telophase I transition, Aurora-C was dephosphorylated and relocalized to the midzone and midbody. Microinjection of the kinase-deficient Aurora-C (AurC-KD) mRNA into mouse oocytes significantly inhibited Aurora-C activity and caused multiple defects, including chromosome misalignment, abnormal kinetochore-microtubule attachment, premature chromosome segregation, and cytokinesis failure in meiosis I. Furthermore, AurC-KD reduced Aurora-C and histone H3 phosphorylation and inhibited kinetochore localization of Bub1 and BubR1. Similar effects also were observed in the oocytes injected with INCNEP-delIN mRNAs, in which the Aurora-C binding motif was removed. The most dramatic effect observed in AurC-KD-injected oocytes is cytokinesis failure in meiosis I, resulting in producing large polyploid oocytes, a pattern similar to Aurora-C deficiency human spermatozoa. Surprisingly, we detected no Aurora-B protein in mouse oocytes. We propose that Aurora-C, but not Aurora-B, plays essential roles in female mouse meiosis.

Comparison of reproductive development in triploid and diploid female rainbow trout Oncorhynchus mykiss

The diploid rainbow trout Oncorhynchus mykiss reached sexual maturity 3 years after hatching and its oogenesis underwent four stages, which were oogonia, primary oocyte, secondary oocyte and egg. Reproductive development and hormone changes of 4 to 35 month-old female O. mykiss were investigated using histological and radioimmunoassay methods in order to provide a theoretical and practical basis for the use of triploid female O. mykiss. The oogonium of the triploid female could develop into the oocytes of the prophase with abortion occurring later; the oogonium was surrounded by stroma cells to form the oogonium cluster and the gonads showed a virilescent tendency when the oogonium clusters were gradually replaced by spermatogenic-like cytocysts. After 13 months, amounts of gonadotropic hormone (GtH-I, GtH-II) and oestradiol (17beta-E(2)) in triploid females were lower than in diploid fish at corresponding time periods, but the amounts of testosterone (T) increased consistently after 21 months and were more than in diploid fish in the corresponding time periods (P > 0.05). The infertility of triploid females resulted from meiosis failure, which caused developmental abortion of oocytes and oogonium formed cytocysts before the prophase oocytes. The cytocyst formation was due to the lack of the normal interaction of ovum and follicular cells, the development of follicular cells producing steroids were inhibited, the arylate path from T to 17beta-E(2) was interrupted, concentration of 17beta-E(2) decreased and concentration of T increased in the blood, the content of vitellogenin (Vg) decreased in the liver with a low 17beta-E(2) and high T caused to ovaries to show a tendency to be virilescent.

Megasporogenesis, Megagametogenesis and Ontogeny of the Aril in Cytisus striatus and C. multiflorus (Leguminosae: Papilionoideae)

There are few embryological reports on wild legumes and even fewer on their seminal appendages. There are no existing studies on the complete ontogeny of these appendages in Cytiseae, a very important Papilionoideae tribe in Mediterranean ecosystems. In this work megasporogenesis, megagametogenesis and aril ontogeny were studied in Cytisus multiflorus and C. striatus, endemics from the western Mediterranean region. Ovaries and ovules from flower buds, flowers at anthesis and hand cross-pollinated flowers were sectioned with a rotary microtome and studied under light and fluorescence microscopy. A monosporic Polygonum-type of megagametogenesis is observed in both species but with megasporogenesis characterized by formation of a triad of cells after incomplete meiosis. The original cell wall of the megaspore mother cell and triad, including the transverse walls between the latter, are surrounded by a callose layer that isolates them from the surrounding diploid tissue; this callose layer gradually disappears during embryo sac formation. There are no antipodals in the mature embryo sac. Aril ontogeny starts in pre-anthesis with the formation of the aril primordium, and its normal development will occur only after fertilization, more specifically after endosperm initiation. After fertilization, a reactivation of meristem capacity takes place in the aril cells resulting in slow and sparse growth. Later, this type of development gradually decreases but the aril cells continue to grow by cell expansion, which in the last period of seed development is the only type of growth of the aril. In the mature seed, the seminal appendage acquires an irregular U-shape in transverse section, showing vacuolated cells with a large central vacuole that stores lipids and some proteins. Meiotic triad formation is due to a failure in meiosis II of the chalazal cell of the dyad. In Cytisus seeds the aril has a funicular origin with predominantly post-fertilization development, but a normal growth of the endosperm is needed for proper aril development.

Mapping diplosporous apomixis in tetraploid Tripsacum: one gene or several genes?

Polyploids in Tripsacum, a wild relative of maize, reproduce through the diplosporous type of apomixis, an asexual mode of reproduction through seeds. Diplosporous apomixis involves both the failure of meiosis and the parthenogenetic development of the unreduced gametes, resulting in progenies that are exact genetic copies of the mother plant. Apomixis is believed to be controlled by one single dominant allele, responsible for the whole developmental process. Construction of a linkage map for the chromosome controlling diplosporous apomixis in Tripsacum was carried out in both tetraploid-apomictic and diploid-sexual Tripsacum species using maize restriction fragment length polymorphism (RFLP) probes. A high level of collinearity was observed between the Tripsacum chromosome carrying the control of apomixis and a duplicated segment in the maize genome. In the apomictic tetraploid, there was a strong restriction to recombination, as compared to the corresponding genomic segment in sexual plants and maize. This suggests that apomixis, although inherited as a single Mendelian allele, might really be controlled by a cluster of linked loci. The analysis also revealed the tetrasomic nature of the inheritance of the chromosomal segment controlling apomixis, which contradicts the usually accepted hypothesis of an allopolyploid origin of apomictic species. The implications of these data for the transfer of apomixis into cultivated crops are discussed, and a new approach to studying the genetics of apomixis, based on comparative mapping, is proposed.