Abscisic acid (ABA) is required for the regulation of seed maturation in maize (Zea mays L.). Mutants blocked in ABA synthesis (such as viviparous-5) do not mature to quiescent, desiccationtolerant seeds, but germinate on the ear midway through kernel development. Because gibberellins (GA) and ABA act antagonistically in many aspects of plant development, we hypothesized that ABA antagonizes a positive GA signal for precocious germination in maize. In these experiments, we show that a GA deficiency early in seed development, induced genetically or via biosynthesis inhibitors, suppresses vivipary in ABA-deficient developing kernels. The resulting seeds have both desiccation tolerance and storage longevity. Temporal analysis of GA accumulation in wild-type kernels revealed the accumulation of bioactive GA 1 and GA 3 prior to the peak in ABA content. We speculate that these GAs stimulate a developmental program leading to vivipary in the absence of normal amounts of ABA, and that a reduction of GA content reestablishes an ABA/GA ratio appropriate for suppression of germination and induction of maturation. In contrast, the induction of a GA deficiency did not suppress vivipary in viviparous-1 mutant kernels, suggesting that VP1 acts downstream of both GA and ABA in programming seed development.
Abscisic acid (ABA) is required for seed maturation in maize (Zea mays L.) and other plants. Gibberellins (GAs) are also present in developing maize embryos, and mutual antagonism of GAs and ABA appears to govern the choice between precocious germination or quiescence and maturation. Exogenous ABA can also induce quiescence and maturation in immature maize embryos in culture. To examine the role of GAs versus ABA in regulating maize embryo maturation, the effects of modulating GA levels were compared with those of ABA in embryos cultured at successive stages of development. The effects of GA synthesis inhibition or exogenous GA application differed markedly in embryos at different stages of development, indicating changes in both endogenous GA levels and in the capacity for GA synthesis as embryogenesis and maturation progress. In immature embryos, the inhibition of GA synthesis mimicked the effects of exogenous ABA, as shown by the suppression of germination, the acquisition of anthocyanin pigments, and the accumulation of a variety of maturation-phase mRNAs. We suggest that GA antagonizes ABA signaling in developing maize embryos, and that the changing hormone balance provides temporal control over the maturation phase.The phytohormone abscisic acid (ABA) plays a variety of roles in plant growth and environmental response, including a critical role in the development of seeds. A rise in the ABA level during embryogenesis triggers processes that lead to the acquisition of desiccation tolerance and seed dormancy. The role of ABA in establishing these characters has been demonstrated by the behavior of mutants that disrupt ABA synthesis or alter ABA sensitivity. In Arabidopsis, mutants that are deficient in ABA synthesis and mutants that are ABA-insensitive show reduced seed maturation and dormancy (Koornneef and Karssen, 1994; Leon-Kloosterziel et al., 1996). In maize (Zea mays L.), many seed-specific ABA responses are due to increases in gene expression that are synergistically regulated by ABA and the transcription factor VP1 (McCarty et al., 1991; Hattori et al., 1992). Mutant maize embryos that are deficient in ABA synthesis or lack an active VP1 factor do not express the normal suite of maturation phase proteins and they do not acquire desiccation tolerance. Unlike in Arabidopsis, these mutants do not become quiescent but germinate precociously on the ear.The timing of Vp1 gene expression and the flux of ABA levels during seed development are not perfectly correlated with the timing of ABA-induced maturation events, suggesting that other modulating factors are also relevant. For example, the induction of the LEA (late embryogenesis abundant protein) genes that are thought to function in desiccation tolerance occurs much later than the time of highest endogenous ABA levels in cotton and maize, although these genes have been shown to require ABA for expression (Galau et al., 1987; Thomann et al., 1992; White and Rivin, 1995). This paradox also extends to the germination behavior of immature maize embryos. ...
Several different types of proteins that are modulated by abscisic acid (ABA) accumulate in developing embryos of maize (Zea mays L.). Some of these proteins are specific to the developing seed, such as the storage globulin, GLB1, whereas others are involved in general responses to water deficit. Here we describe a maize protein family of this second type, a Group 3 late embryogenesis abundant (MLG3). Like other proteins of this class, MLG3 polypeptides are ABA-responsive. They are found in maturing seeds and in dehydrating plant tissues. Antigenically related proteins are found in other cereals. To distinguish the regulation of developmentally programmed ABA responses from those that are environmentally induced, we compared the ontological pattem and accumulation requirements of MLG3 polypeptides with those we previously described for GLB1. GLB1 accumulation begins early in the maturation phase and specifically requires high levels of ABA and the participation of the Viviparous-I (Vpl) gene product. Vpl is required for other ABA-modulated events in maize seed development as well. In experiments using vpl mutants and mutants deficient in ABA synthesis (vp5 mutation), we show that MLG3 accumulation also is dependent upon ABA, but it shows striking differences from GLBI. MLG3 accumulates much later in embryogenesis, coincident with the onset of dehydration. In contrast to GLBI, MLG3 proteins can be induced by de novo ABA synthesis in response to culturing in high osmoticum. Unlike GLB1, MLG3 has no specific requirement for the Vpl gene product.
Prolapsed nictitans gland (PNG) is an important ocular condition of dogs. Various surgical interventions have been described, but effective technique is currently considered to be a matter of personal clinician preference. The aim of this rapid review was to evaluate existing peer-reviewed evidence of effectiveness for surgical techniques and their subsequent effects on quantitative and clinical lacrimal outcomes for PNG. We performed a structured bibliographic search of CAB Abstracts, PubMed, and Medline using terms relevant to dogs, nictitans gland, and surgery on 13 September 2017. Included studies were assessed for study design, reporting characteristics, surgical techniques, and surgical and lacrimal outcomes. Fifteen of three hundred fifteen identified studies were eligible for inclusion. Seven different replacement techniques were identified, along with gland excision. All studies were observational or descriptive, with the exception of a single crossover trial. Outcomes reporting was heterogeneous and provided limited detail on lacrimal outcomes or on breed propensity for recurrence. Insufficient data precluded comparison of techniques for either surgical failure rates or lacrimal outcomes, although proportional meta-analysis yielded an overall failure rate of 3% (95% CI 1–7%) for the Morgan’s pocket procedure. Improved reporting of veterinary surgical studies will improve evidence appraisal and synthesis, as well as reduce potential sources of bias.
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