Overdominant lethals as part of the conifer embryo lethal system

In pines, self-pollination rates can be as high as 34% yet only 5% of viable seed is a product of self-fertilization. This decline in selfed seed viability is the consequence of post-fertilization exclusion mechanisms operating via the embryo lethal system. Recent molecular marker dissection studies suggest that the embryo lethal system is composed of semilethal factors dispersed across the genome, but it is not clear whether overdominant lethal factors are rare or representative. The study objective was to determine if overdominance was rare for the embryo lethal system in conifers. Three cohorts of selfed offspring from a single Pinus taeda parent were genotyped for nuclear microsatellites. Maximum likelihood tests based on distorted segregation ratios for single markers and for interval mapping were used to infer the degree of dominance. Four hypotheses about overdominance lethal factors were tested: (1) overdominant lethal factors rarely occur within the embryo lethal system, (2) overdominant lethal factors are rarely detected because they are transient and display stage-specific expression, (3) overdominant lethal factors are rarely detected due to tight linkage with rare marker alleles and (4) dominance estimation is unbiased by gametic selection. Four out of the seven chromosomal segments were linked to an overdominant lethal factor. One of these four segments had symmetric overdominance, an effect which persisted from embryo maturity through germination. Four overdominant lethal factors were linked to common and rare marker alleles. Gametic selection was not a source of bias in dominance estimation. Overdominant or pseudo-overdominant lethal factors are a common component of the conifer embryo lethal system.     

Production of haploids and doubled haploids in oil palm

Background

Studies on host-pathogen interactions in a range of pathosystems have revealed an array of mechanisms by which plants reduce the efficiency of pathogenesis. While R-gene mediated resistance confers highly effective defense responses against pathogen invasion, quantitative resistance is associated with intermediate levels of resistance that reduces disease progress. To test the hypothesis that specific loci affect distinct stages of fungal pathogenesis, a set of maize introgression lines was used for mapping and characterization of quantitative trait loci (QTL) conditioning resistance to Setosphaeria turcica, the causal agent of northern leaf blight (NLB). To better understand the nature of quantitative resistance, the identified QTL were further tested for three secondary hypotheses: (1) that disease QTL differ by host developmental stage; (2) that their performance changes across environments; and (3) that they condition broad-spectrum resistance.

Results

Among a set of 82 introgression lines, seven lines were confirmed as more resistant or susceptible than B73. Two NLB QTL were validated in BC₄F₂ segregating populations and advanced introgression lines. These loci, designated qNLB1.02 and qNLB1.06, were investigated in detail by comparing the introgression lines with B73 for a series of macroscopic and microscopic disease components targeting different stages of NLB development. Repeated greenhouse and field trials revealed that qNLB1.06 _Tx303 (the Tx303 allele at bin 1.06) reduces the efficiency of fungal penetration, while qNLB1.02 _B73 (the B73 allele at bin 1.02) enhances the accumulation of callose and phenolics surrounding infection sites, reduces hyphal growth into the vascular bundle and impairs the subsequent necrotrophic colonization in the leaves. The QTL were equally effective in both juvenile and adult plants; qNLB1.06 _Tx303 showed greater effectiveness in the field than in the greenhouse. In addition to NLB resistance, qNLB1.02 _B73 was associated with resistance to Stewart's wilt and common rust, while qNLB1.06 _Tx303 conferred resistance to Stewart's wilt. The non-specific resistance may be attributed to pleiotropy or linkage.

Conclusions

Our research has led to successful identification of two reliably-expressed QTL that can potentially be utilized to protect maize from S. turcica in different environments. This approach to identifying and dissecting quantitative resistance in plants will facilitate the application of quantitative resistance in crop protection.     

Differential mechanisms of x-ray-induced cell death in human endothelial progenitor cells isolated from cord blood and adults

Endothelial colony-forming cells (ECFCs) are endothelial progenitor cells that circulate at low concentration in human umbilical cord and adult peripheral blood and are largely resident in blood vessels. ECFCs not only appear to be critical for normal vascular homeostasis and repair but may also contribute to tumor angiogenesis and response to therapy. To begin to characterize the potential role of ECFCs during the treatment of tumors in children and adults with radiation, we characterized the X-ray sensitivity of cord and adult blood-derived ECFCs. We found both cord blood and adult ECFCs to be highly radiation sensitive (3 Gy resulted in >90% killing without induction of apoptosis). The X-ray survival curves suggested reduced potential for repair capacity, but X-ray fractionation studies demonstrated that all the ECFCs exhibited repair when the radiation was fractionated. Finally, the mechanisms of X-ray-induced cell death for cord blood and adult ECFCs were different at low and high dose. At low dose, all ECFCs appear to die by mitotic death/catastrophe. However, at high radiation doses (≥ 10 Gy) cord blood ECFCs underwent p53 stabilization and Bax-dependent apoptosis as well as p21-dependent G? and G?/M cell cycle checkpoints. By contrast, after 10 Gy adult ECFCs undergo only large-scale radiation-induced senescence, which is a cellular phenotype linked to premature development of atherosclerosis and vasculopathies. These data demonstrate that the ECFC response to radiation is dose-dependent and developmentally regulated and may provide potential mechanistic insight into their role in tumor and normal tissue response after ionizing radiation treatment.     

Genetic regulation of embryo death and senescence

The survival of the preimplantation mammalian embryo depends not only on providing the proper conditions for normal development but also on acquiring the mechanisms by which embryos cope with adversity. The ability of the early conceptus to resist stress as development proceeds may be regulated by diverse factors such as the attainment of a cell death program and protective mechanisms involving stress-induced genes and/or cell cycle modulators. This paper reviews the recent research on the genetic regulation of early embryo cell death and senescence focussing on the bovine species where possible. The different modes of cell death will be explained, clarifying the confusing cell death terminology, by advocating the recommendations set forth by the Cell Death Nomenclature Committee to extend to the embryology research field. Specific pro-death and anti-death genes will be discussed with reference to their expression patterns during early mammalian embryogenesis.     

Excess of heterozygotes at albumin locus in American Standardbred horses

Summary. Data from 5934 matings of American Standardbred horses provided evidence for an excess of heterozygotes at the albumin locus, statistically significant ( P <0.01) in one mating class (A1-AB stallions x A1-A dams), primarily attributed to an excess of heterozygotes among male offspring.     

Role of luteal regression in embryo death in cattle

Inseminated crossbred beef cows and heifers were used in 2 experiments to investigate embryo survival after prostaglandin-induced or spontaneous luteal regression. In Experiment 1, luteal regression was induced by an intramuscular (im) injection of cloprostenol (500 mug) on Day 15 (day of ovulation = Day 0). Progestagen was replaced 24 or 36 h later either by one-and-a-half Syncro-Mate-B (SMB) ear implants (9 mg of norgestomet) and norgestomet solution (2.25 mg, im) containing no estradiol in 1 replicate or by 2 SMB implants (12 mg of norgestomet) and progesterone (100 mg, im) in the second replicate. Combined for both replicates, the Day-24 pregnancy rate in an untreated control group (Group 1, 16/19; 84%) was higher (P < 0.01) than in the 24-h group (Group 2, 9/20; 45%), which also was higher (P < 0.02) than in the 36-h group (Group 3, 3/23; 13%). In Experiment 2, 15 or 16 d after breeding, cattle with a corpus luteum at least 16 x 16 mm were given either 2 SMB implants or no treatment. At 24 to 26 d after breeding, pregnancy rates (48/65, 74% versus 49/68, 72%) were not significantly different, and all but 1 of the pregnant progestagen-supplemented cattle had a functional corpus luteum.     

Cell death in development: shaping the embryo

Cell death in animals is normally classified as type I (apoptotic), type II (autophagic) or necrotic. Of the biologically controlled types of death, in most embryos apoptosis is the most common, although in metamorphosis and in cells with massive cytoplasm type II is often seen, and intermediate forms are seen. For vertebrate embryos other than mammals, apoptosis is not seen prior to gastrulation but thereafter is used to sculpt the organs of the embryo, while overproduction of cells with subsequent death of excess cells is a common means of generating high specificity with low information cost. In zebrafish at least, the inability of embryos prior to the maternal-zygotic transition to undergo apoptosis appears to derive from the inability of the cells to resist lysis once apoptosis begins, rather than any inhibition of apoptosis. In mammalian embryos, apoptosis is seen during cavitation. Thereafter, as in other embryos, cell death plays a major role in shaping and sculpting the embryo. In those situations that have been carefully studied, cell death is under tight genetic control (including regulation of gene products whose function in cell death is not yet known, such as cdk5), with activation of apoptosis sometimes regulated by local environmental variables.     

Stages in the development of the embryo of the fresh-water crayfishCherax destructor

Summary Development of the crayfish embryo is described in sequential stages separated by intervals that represent 5% of the total time taken from fertilization to hatching, which is 40 days at 19° C. Early cell division, aggregation of blastoderm cells into the ventral plate, gastrulation and formation of the embryo can be clearly observed through the transparent chorion and each stage characterised using morphological criteria. At hatching the egg chorion splits open but the hatchling (postembryo stage 1) remains attached to the inside of the egg by membranes extending from its tail. 7 to 8 days later the hatchling moults to produce the 2nd post-embryonic stage. Free from the egg, it still clings to the mother. 14 days later the 2nd postembryonic stage moults to produce the immature adult.