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Following tuber induction, potato tubers undergo a period of dormancy during which visible bud growth is inhibited. The length of the dormancy period is under environmental, physiological and hormonal control. Sucrose availability is one prerequisite for bud break. In the absence of sucrose, no bud break occurs. Thus, sucrose is likely to serve as nutrient and signal molecule at the same time. The mode of sucrose sensing is only vaguely understood, but most likely involves trehalose-6-phosphate and SnRK1 signalling networks. This conclusion is supported by the observation that ectopically manipulation of trehalose-6-phosphate levels influences the length of the dormancy period. Once physiological competence is achieved, sprouting is controlled by the level of phytohormones. Two phytohormones, ABA and ethylene, are supposed to suppress tuber sprouting; however, the exact role of ethylene remains to be elucidated. Cytokinins and gibberellins are required for bud break and sprout growth, respectively. The fifth classical phytohormone, auxin, seems to play a role in vascular development. During the dormancy period, buds are symplastically isolated, which changes during bud break. In parallel to the establishment of symplastic connectivity, vascular tissue develops below the growing bud most likely to support the outgrowing sprout with assimilates mobilised in parenchyma cells. Sprouting leads to major quality losses of stored potato tubers. Therefore, control of tuber sprouting is a major objective in potato breeding. Although comparative transcriptome analysis revealed a large number of genes differentially expressed in growing versus dormant buds, no master-regulator of potato tuber sprouting has been identified so far.

• Pre-harvest sprouting (PHS), the germination of grain before harvest, is a serious problem resulting in wheat yield and quality losses. • Here, we mapped the PHS resistance gene PHS-3D from synthetic hexaploid wheat to a 2.4 Mb presence–absence variation (PAV) region and found that its resistance effect was attributed to the pleiotropic Myb10-D by integrated omics and functional analyses. • Three haplotypes were detected in this PAV region among 262 worldwide wheat lines and 16 Aegilops tauschii, and the germination percentages of wheat lines containing Myb10-D was approximately 40% lower than that of the other lines. Transcriptome and metabolome profiling indicated that Myb10-D affected the transcription of genes in both the flavonoid and abscisic acid (ABA) biosynthesis pathways, which resulted in increases in flavonoids and ABA in transgenic wheat lines. Myb10-D activates 9-cis-epoxycarotenoid dioxygenase (NCED) by biding the secondary wall MYB-responsive element (SMRE) to promote ABA biosynthesis in early wheat seed development stages. • We revealed that the newly discovered function of Myb10-D confers PHS resistance by enhancing ABA biosynthesis to delay germination in wheat. The PAV harboring Myb10-D associated with grain color and PHS will be useful for understanding and selecting white grained PHS resistant wheat cultivars.

• In cereal crops, ABA deficiency during seed maturation phase causes pre-harvest sprouting (PHS), and molybdenum cofactor (MoCo) is required for ABA biosynthesis. • Here, two rice PHS mutants F254 and F5-1 were characterized. In addition to the PHS, these mutants showed pleiotropic phenotypes such as twisting and slender leaves, and then died when the seedling developed to four or five leaves. Map-based cloning showed that OsCNX6 and OsCNX1 encoding homologs of MoaE and MoeA were responsible for F254 and F5-1 mutants, respectively. Genetic complementation indicated that OsCNX6 not only rescued the PHS and seedling lethal phenotype of the cnx6 mutant, but also recovered the MoCo-dependent enzyme activities such as xanthine dehydrogenase (XDH), aldehyde oxidase (AO), nitrate reductase (NR) and sulfite oxidase (SO). • Expression pattern showed that OsCNX6 was richly expressed in seed during embryo maturation by quantitative reverse transcriptase PCR and RNA in situ hybridization. Furthermore, the OsCNX6 overexpression plants can significantly enhance the MoCo-dependent enzyme activities, and improved the osmotic and salt stress tolerance without unfavorable phenotypes. • Collectively, these data indicated that OsCNX6 participated in MoCo biosynthesis, and is essential for rice development, especially for seed dormancy and germination, and OsCNX6 could be an effective target for improving abiotic stress tolerance in rice.

The cellular basis of age-related behavioral decline remains obscure but alterations in synapses are likely candidates. Accordingly, the beneficial effects on neural function of caloric restriction and exercise, which are among the most effective anti-aging treatments known, might also be mediated by synapses. As a starting point in testing these ideas, we studied the skeletal neuromuscular junction (NMJ), a large, accessible peripheral synapse. Comparison of NMJs in young adult and aged mice revealed a variety of age-related structural alterations, including axonal swellings, sprouting, synaptic detachment, partial or complete withdrawal of axons from some postsynaptic sites, and fragmentation of the postsynaptic specialization. Alterations were significant by 18 mo of age and severe by 24 mo. A life-long calorie-restricted diet significantly decreased the incidence of pre- and postsynaptic abnormalities in 24-mo-old mice and attenuated age-related loss of motor neurons and turnover of muscle fibers. One month of exercise (wheel running) in 22-mo-old mice also reduced age-related synaptic changes but had no effect on motor neuron number or muscle fiber turnover. Time-lapse imaging in vivo revealed that exercise partially reversed synaptic alterations that had already occurred. These results demonstrate a critical effect of aging on synaptic structure and provide evidence that interventions capable of extending health span and lifespan can partially reverse these age-related synaptic changes.

As in other cultivated species, dormancy can be seen as a problem in cereal production, either due to its short duration or to its long persistence. Indeed, cereal crops lacking enough dormancy at harvest can be exposed to pre-harvest sprouting damage, while a long-lasting dormancy can interfere with processes that rely on rapid germination, such as malting or the emergence of a uniform crop. Because the ancestors of cereal species evolved under very diverse environments worldwide, different mechanisms have arisen as a way of sensing an appropriate germination environment (a crucial factor for winter or summer annuals such as cereals). In addition, different species (and even different varieties within the same species) display diverse grain morphology, allowing some structures to impose dormancy in some cereals but not in others. As in seeds from many other species, the antagonism between the plant hormones abscisic acid and gibberellins is instrumental in cereal grains for the inception, expression, release and re-induction of dormancy. However, the way in which this antagonism operates is different for the various species and involves different molecular steps as regulatory sites. Environmental signals (i.e. temperature, light quality and quantity, oxygen levels) can modulate this hormonal control of dormancy differently, depending on the species. The practical implications of knowledge accumulated in this field are discussed.

Pre-harvest sprouting (PHS) causes serious damage that leads to deterioration in overall quality and decreased yield and reduction of grain yield in cereal. In this study, two major quantitative trait loci (QTLs), qPHS.sicau-3D and qPHS.sicau-1B , were detected in synthetic wheat (SHW-L1) and were derived from Aegilops tauschii AS60 (deep dormant) and Triticum turgidum AS2255 (medium PHS-resistant). qPHS.sicau-1B is located in the region near the telomere of 1BS, and qPHS.sicau-3D is located on the end of 3DL; these QTLs explain approximately 20.99% and 42.47% of the phenotypic variation. Pyramiding of both QTLs showed superior PHS resistance in recombinant inbred lines (RILs). The array-based SNP markers AX-94924265 for qPHS.sicau-1B and AX-94415259 for qPHS.sicau-3D were successfully converted to Kompetitive Allele Specific Polymerase Chain Reaction (KASP) and STS markers. L10-1580 is a light red breeding materials selected from SHW-L1-derived breeding lines that harbors the PHS-tolerant elite alleles which showed similar germination level with SHW-L1 and better resistance than other common wheat parents. L10-1580 harbors the elite alleles AX-94924265_GG/AX-94415259_B which showed similar PHS resistance as SHW-L1 and better resistance than other common wheat parents. Therefore, these QTLs for PHS resistance obtained from synthetic wheat could combine or coexist with other elite agronomic traits in high-yield wheat cultivars.

Preharvest sprouting (PHS) and late maturity α-amylase (LMA) are the two major causes of unacceptably high levels of α-amylase in ripe wheat grain. High α-amylase activity in harvested grain results in substantially lower prices for wheat growers and at least in the case of PHS, is associated with adverse effects on the quality of a range of end-products and loss of viability during storage. The high levels of α-amylase are reflected in low falling number, the internationally accepted measure for grain receival and trade. Given the significant losses that can occur, elimination of these defects remains a major focus for wheat breeding programs in many parts of the world. In addition, the genetic, biochemical and molecular mechanisms involved in the control of PHS and LMA as well as the interactions with environmental factors have attracted a sustained research interest. PHS and LMA are independent, genetically controlled traits that are strongly influenced by the environment, where the effects of particular environmental factors vary substantially depending on the stage of grain development and ripening. This review is a summary and an assessment of results of recent research on these important grain quality defects.

Background Pre-harvest sprouting (PHS) in wheat can cause substantial reduction in grain yield and end-use quality. Grain color (GC) together with other components affect PHS resistance. Several quantitative trait loci (QTL) have been reported for PHS resistance, and two of them on chromosome 3AS ( TaPHS1 ) and 4A have been cloned. Methods To determine genetic architecture of PHS and GC and genetic relationships of the two traits, a genome-wide association study (GWAS) was conducted by evaluating a panel of 185 U.S. elite breeding lines and cultivars for sprouting rates of wheat spikes and GC in both greenhouse and field experiments. The panel was genotyped using the wheat 9K and 90K single nucleotide polymorphism (SNP) arrays. Results Four QTL for GC on four chromosomes and 12 QTL for PHS resistance on 10 chromosomes were identified in at least two experiments. QTL for PHS resistance showed varied effects under different environments, and those on chromosomes 3AS, 3AL, 3B, 4AL and 7A were the more frequently identified QTL. The common QTL for GC and PHS resistance were identified on the long arms of the chromosome 3A and 3D. Conclusions Wheat grain color is regulated by the three known genes on group 3 chromosomes and additional genes from other chromosomes. These grain color genes showed significant effects on PHS resistance in some environments. However, several other QTL that did not affect grain color also played a significant role on PHS resistance. Therefore, it is possible to breed PHS-resistant white wheat by pyramiding these non-color related QTL.

Background When the homeostasis of the central nervous system (CNS) is altered, microglial cells become activated displaying a wide range of phenotypes that depend on the specific site, the nature of the activator, and particularly the microenvironment generated by the lesion. Cytokines are important signals involved in the modulation of the molecular microenvironment and hence play a pivotal role in orchestrating microglial activation. Among them, interleukin-6 (IL-6) is a pleiotropic cytokine described in a wide range of pathological conditions as a potent inducer and modulator of microglial activation, but with contradictory results regarding its detrimental or beneficial functions. The objective of the present study was to evaluate the effects of chronic IL-6 production on the immune response associated with CNS-axonal anterograde degeneration. Methods The perforant pathway transection (PPT) paradigm was used in transgenic mice with astrocyte-targeted IL6-production (GFAP-IL6Tg). At 2, 3, 7, 14, and 21 days post-lesion, the hippocampal areas were processed for immunohistochemistry, flow cytometry, and protein microarray. Results An increase in the microglia/macrophage density was observed in GFAP-IL6Tg animals in non-lesion conditions and at later time-points after PPT, associated with higher microglial proliferation and a major monocyte/macrophage cell infiltration. Besides, in homeostasis, GFAP-IL6Tg showed an environment usually linked with an innate immune response, with more perivascular CD11b + /CD45 high /MHCII + /CD86 + macrophages, higher T cell infiltration, and higher IL-10, IL-13, IL-17, and IL-6 production. After PPT, WT animals show a change in microglia phenotype expressing MHCII and co-stimulatory molecules, whereas transgenic mice lack this shift. This lack of response in the GFAP-IL6Tg was associated with lower axonal sprouting. Conclusions Chronic exposure to IL-6 induces a desensitized phenotype of the microglia.