A map of the barley genome consisting of 295 loci was constructed. These loci include 152 cDNA restriction fragment length polymorphism (RFLP), 114 genomic DNA RFLP, 14 random amplified polymorphic DNA (RAPD), five isozyme, two morphological, one disease resistance and seven specific amplicon polymorphism (SAP) markers. The RFLP-identified loci include 63 that were detected using cloned known function genes as probes. The map covers 1,250 centiMorgans (cM) with a 4.2 cM average distance between markers. The genetic lengths of the chromosomes range from 124 to 223 cM and are in approximate agreement with their physical lengths. The centromeres were localized to within a few markers on all of the barley chromosomes except chromosome 5. Telomeric regions were mapped for the short (plus) arms of chromosomes 1, 2 and 3 and the long (minus) arm of chromosomes 7.

SUMMARY Although mature myocytes rely on mitochondria as the primary source of energy, the role of mitochondria in the developing heart is not well known. Here, we find closure of the mitochondrial permeability transition pore (mPTP) drives maturation of mitochondrial structure and function and myocyte differentiation. Cardiomyocytes at embryonic day (E) 9.5, when compared to E13.5, displayed fragmented mitochondria with few cristae, a less polarized mitochondrial membrane potential, higher reactive oxygen species (ROS) levels, and an open mPTP. Pharmacologic and genetic closing of the mPTP yielded maturation of mitochondrial structure and function, lowered ROS, and increased myocyte differentiation (measured by counting Z-bands). Furthermore, myocyte differentiation was inhibited and enhanced with oxidant and antioxidant treatment, respectively, suggesting that redox signaling pathways lie downstream of mitochondria to regulate cardiac myocyte differentiation.

Summary Objective:  The current review describes how the health status profile of people with fibromyalgia (FM) compares to that of people in the general population and patients with other health conditions. Methods:  A review of 37 studies of FM that measured health status with the 36‐item Medical Outcomes Study Short‐Form Health Survey (SF‐36) or the 12‐item Short‐Form Health Survey (SF‐12). Results:  Studies performed worldwide showed that FM groups were significantly more impaired than people in the general population on all eight health status domains assessed. These domains include physical functioning, role functioning difficulties caused by physical problems, bodily pain, general health, vitality (energy vs. fatigue), social functioning, role functioning difficulties caused by emotional problems and mental health. FM groups had mental health summary scores that fell 1 standard deviation (SD) below the general population mean, and physical health summary scores that fell 2 SD below the general population mean. FM groups also had a poorer overall health status compared to those with other specific pain conditions. FM groups had similar or significantly lower (poorer) physical and mental health status scores compared to those with rheumatoid arthritis, osteoarthritis, osteoporosis, systemic lupus erythematosus, myofacial pain syndrome, primary Sjögren's syndrome and others. FM groups scored significantly lower than the pain condition groups mentioned above on domains of bodily pain and vitality. Health status impairments in pain and vitality are consistent with core features of FM. Conclusions:  People with FM had an overall health status burden that was greater in magnitude compared to people with other specific pain conditions that are widely accepted as impairing.

Molecular mapping of cultivated oats was conducted to update the previous reference map constructed using a recombinant inbred (RI) population derived from Avena byzantina C. Koch cv. Kanota x Avena sativa L. cv. Ogle. In the current work, 607 new markers were scored, many on a larger set of RI lines (133 vs. 71) than previously reported. A robust, updated framework map was developed to resolve linkage associations among 286 markers. The remaining 880 markers were placed individually within the most likely framework interval using chi2 tests. This molecular framework incorporates and builds on previous studies, including physical mapping and linkage mapping in additional oat populations. The resulting map provides a common tool for use by oat researchers concerned with structural genomics, functional genomics, and molecular breeding.

Quantitative trait locus (QTL) main effects and QTL by environment (QTL × E) interactions for seven agronomic traits (grain yield, days to heading, days to maturity, plant height, lodging severity, kernel weight, and test weight) were investigated in a two-row barley (Hordeura vulgare L.) cross, Harrington/TR306. A 127-point base map was constructed from markers (mostly RFLP) scored in 146 random double-haploid (DH) lines from the Harrington/TR306 cross. Field experiments involving the two parents and 145 random DH lines were grown in 1992 and/or 1993 at 17 locations in North America. Analysis of QTL was based on simple and composite interval mapping. Primary QTL were declared at positions where both methods gave evidence for QTL. The number of primary QTL ranged from three to six per trait, collectively explaining 34 to 52% of the genetic variance. None of these primary QTL showed major effects, but many showed effects that were consistent across environments. The addition of secondary QTL gave models that explained 39 to 80% of the genetic variance. The QTL were dispersed throughout the barley genome and some were detected in regions where QTL have been found in previous studies. Eight chromosome regions contained pleiotropic loci and/or linked clusters of loci that affected multiple traits. One region on chromosome 7 affected all traits except days to heading. This study was an intensive effort to evaluate QTL in a narrow-base population grown in a large set of environments. The results reveal the types and distributions of QTL effects manipulated by plant breeders and provide opportunities for future testing of marker-assisted selection. M OLECULAR MAPS of plant genomes, used in conjunction with phenotypic measurements, can provide information about chromosome regions that affect quantitative traits. Although knowing whether such regions represent individual quantitative trait loci (QTL)

Hoffman DL, Salter JD, Brookes PS. Response of mitochondrial reactive oxygen species generation to steady-state oxygen tension: implications for hypoxic cell signaling. Am J Physiol Heart Circ Physiol 292: H101-H108, 2007. First published September 8, 2006; doi:10.1152/ajpheart.00699.2006.-Mitochondria are proposed to play an important role in hypoxic cell signaling. One currently accepted signaling paradigm is that the mitochondrial generation of reactive oxygen species (ROS) increases in hypoxia. This is paradoxical, because oxygen is a substrate for ROS generation. Although the response of isolated mitochondrial ROS generation to [O 2] has been examined previously, such investigations did not apply rigorous control over [O2] within the hypoxic signaling range. With the use of open-flow respirometry and fluorimetry, the current study determined the response of isolated rat liver mitochondrial ROS generation to defined steady-state [O2] as low as 0.1 M. In mitochondria respiring under state 4 (quiescent) or state 3 (ATP turnover) conditions, decreased ROS generation was always observed at low [O 2]. It is concluded that the biochemical mechanism to facilitate increased ROS generation in response to hypoxia in cells is not intrinsic to the mitochondrial respiratory chain alone but may involve other factors. The implications for hypoxic cell signaling are discussed.hypoxia-inducible factor; superoxide; free radicals; mitochondria; metabolism REACTIVE OXYGEN SPECIES (ROS) generated by mitochondria are key intermediates in a diverse array of cell signaling events, including regulation of the cell cycle (68), proliferation (51), metalloproteinases (65), apoptosis (54), protein kinases (8,16,54,64), phosphatases (62), growth factor signaling (78), and transcription factors (44, 52) (see Ref. 31 for review). One area of investigation that has been the focus of much recent interest is the potential role of mitochondrial ROS in the signaling events that occur during hypoxia, including the regulation of hypoxia-inducible factors such as HIF-1␣ (2, 4, 7, 10, 25, 32, 48, 56, 59, 67, 84 -86, 88, 89). Whereas the downstream effects of mitochondrially derived ROS are relatively well established (vide supra), the mechanisms and the directionality (i.e., increased or decreased) of mitochondrial ROS generation in hypoxia are currently under debate (59,86). This is an important area of study, since it appears that not only can mitochondria regulate HIF, but HIF and its downstream target genes (e.g., heme oxygenase) are important pathophysiological regulators of mitochondrial function (5, 42, 77). Thus, perturbing the mitochondria/HIF signaling loop may contribute to disease pathogenesis (10).A widely accepted model of hypoxic cell signaling is that mitochondrial ROS generation increases in hypoxia (7,25,32,67,85,86,88,89). This is proposed to occur via O 2 limitation at the terminal enzyme in the mitochondrial respiratory chain, cytochrome c oxidase (complex IV), causing a backup of electrons in the proximal chain and increase...

Cardiac metabolism is finely tuned, and disruption of myocardial bioenergetics can be clinically devastating. Many cardiomyopathies that present early in life are due to disruption of the maturation of these metabolic pathways. However, this bioenergetic maturation begins well before birth, when the embryonic heart is first beginning to beat, and continues into the mature animal. Thus, the changes in energy production seen after birth are actually part of a continuum that coincides with the structural and functional changes that occur as the cardiac myocyte differentiates and the heart undergoes morphogenesis. Therefore, although bioenergetics and mitochondrial biology have not been studied in great detail in the developing heart, bioenergetic maturation should be considered an important component of normal myocyte differentiation. Although events occurring after birth will be discussed, this review will focus on the changes in bioenergetics and mitochondrial biology that coincide with myocyte differentiation and cardiac morphogenesis. The relationship of these changes to the etiology and presentation of cardiomyopathies will be used as a starting point for this discussion. Then, after reviewing cardiac development and mitochondrial biology, the published data on bioenergetics and mitochondrial structure and function in the developing heart will be presented. Finally, the case will be made that mitochondria may be critical regulators of cardiac myocyte differentiation and cardiac development.

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