Auxin polar transport is essential for the development of zygote and embryo in Nicotiana tabacum L. and correlated with ABP1 and PM H+-ATPase activities

Auxin is an important plant growth regulator, and plays a key role in apical–basal axis formation and embryo differentiation, but the mechanism remains unclear. The level of indole-3-acetic acid (IAA) during zygote and embryo development of Nicotiana tabacum L. is investigated here using the techniques of GC-SIM-MS analysis, immunolocalization, and the GUS activity assay of DR5::GUS transgenic plants. The distribution of ABP1 and PM H+-ATPase was also detected by immunolocalization, and this is the first time that integral information has been obtained about their distribution in the zygote and in embryo development. The results showed an increase in IAA content in ovules and the polar distribution of IAA, ABP1, and PM H+-ATPase in the zygote and embryo, specifically in the top and basal parts of the embryo proper (EP) during proembryo development. For information about the regulation mechanism of auxin, an auxin transport inhibitor TIBA (2,3,5-triiodobenzoic acid) and exogenous IAA were, respectively, added to the medium for the culture of ovules at the zygote and early proembryo stages. Treatment with a suitable IAA concentration promoted zygote division and embryo differentiation, while TIBA treatment obviously suppressed these processes and caused the formation of abnormal embryos. The distribution patterns of IAA, ABP1, and PM H+-ATPase were also disturbed in the abnormal embryos. These results indicate that the polar distribution and transport of IAA begins at the zygote stage, and affects zygote division and embryo differentiation in tobacco. Moreover, ABP1 and PM H+-ATPase may play roles in zygote and embryo development and may also be involved in IAA signalling transduction

Integrating the Genetic and Physical Maps of Arabidopsis thaliana: Identification of Mapped Alleles of Cloned Essential (EMB) Genes

The classical genetic map of Arabidopsis includes more than 130 genes with an embryo-defective (emb) mutant phenotype. Many of these essential genes remain to be cloned. Hundreds of additional EMB genes have been cloned and catalogued (www.seedgenes.org) but not mapped. To facilitate EMB gene identification and assess the current level of saturation, we updated the classical map, compared the physical and genetic locations of mapped loci, and performed allelism tests between mapped (but not cloned) and cloned (but not mapped) emb mutants with similar chromosome locations. Two hundred pairwise combinations of genes located on chromosomes 1 and 5 were tested and more than 1100 total crosses were screened. Sixteen of 51 mapped emb mutants examined were found to be disrupted in a known EMB gene. Alleles of a wide range of published EMB genes (YDA, GLA1, TIL1, AtASP38, AtDEK1, EMB506, DG1, OEP80) were discovered. Two EMS mutants isolated 30 years ago, T-DNA mutants with complex insertion sites, and a mutant with an atypical, embryo-specific phenotype were resolved. The frequency of allelism encountered was consistent with past estimates of 500 to 1000 EMB loci. New EMB genes identified among mapped T-DNA insertion mutants included CHC1, which is required for chromatin remodeling, and SHS1/AtBT1, which encodes a plastidial nucleotide transporter similar to the maize Brittle1 protein required for normal endosperm development. Two classical genetic markers (PY, ALB1) were identified based on similar map locations of known genes required for thiamine (THIC) and chlorophyll (PDE166) biosynthesis. The alignment of genetic and physical maps presented here should facilitate the continued analysis of essential genes in Arabidopsis and further characterization of a broad spectrum of mutant phenotypes in a model plant

An Acute Respiratory Infection of a Physiologically Anemic Infant is a More Likely Cause of SIDS than Neurological Prematurity

Introduction: The cause of the Sudden Infant Death Syndrome (SIDS) is perhaps the oldest of unsolved mysteries of medicine, possibly dating back to Exodus in Biblical times when Egyptian children died in their sleep as if from a plague. It occurs when infants die unexpectedly with no sufficient cause of death found in a forensic autopsy including death scene investigation and review of medical history. That SIDS is an X-linked recessive death from infectious respiratory disease of a physiologically anemic infant and not a simple anomalous cardiac or neurological condition is an extraordinary claim that requires extraordinary evidence. If it were by a simple cause it would have been solved already with over 11,000 papers on SIDS listed now in PUBMED. Any proposed cause of SIDS must explain: 1) its 50% excess male death rate; 2) its 4-parameter lognormal distribution of ages at death; 3) its winter maxima and summer minima; and 4) its increasing rate with livebirth order.Methods: From extensive SIDS vital statistics data and published epidemiologic studies, we developed probability models to explain the mathematical behavior of SIDS meeting the four constraints mentioned above. We then compare these SIDS properties to infant death from Acute Respiratory Infection (ARI), and infant death from Encephalopathy, Unspecified (EU).Results: Comparisons show that SIDS are congruent with ARI and are not consistent with EU, and that these probability models not only fit the SIDS data but they also predict and fit the male fraction of all infant and child mortality from birth through the first 5 years of their life.Conclusions: SIDS are not rejected as an X-linked disease involving ARI and are not explained by a triple risk model that has been commonly accepted by the SIDS medical community as implicating a neurological causation process in a subset of SIDS

A New Bottle Design Decreases Hypoxemic Episodes during Feeding in Preterm Infants

Oxygen saturation is lower during bottle feeding than during breastfeeding in preterm infants. Our objective was to compare two different bottle systems in healthy preterm infants before discharge in terms of SpO2 and oral feeding efficiency (rate of milk intake). Infants without supplement oxygen needs were evaluated twice on the same day during two consecutive feeds, by the same nurse. Infants served as their own controls for comparison of two systems of bottles, the order of which was randomized. The new bottle's nipple design mimics mom's breast in shape and feel, and the bottle vents to air when the child sucks on the nipple. The other system was the hospital's standard plastic bottle with silicone nipple. The rate of milk intake was calculated as the total volume transferred minus volume lost divided by time of feeding, mL/min. Thirty-four infants (BW: 1,163±479.1 g) were studied at 35.4±1.3 weeks after-conception. SpO2 was significantly higher in infants fed with the new bottle design. Milk intake rate was significantly higher with the new bottle than with the standard bottle design. The new bottle design improves oral feeding performance in preterm infants near to discharge when compared to that of a standard bottle