Towards an understanding of the role of intrinsic protein disorder on plant adaptation to environmental challenges

Intrinsic protein disorder is an interesting structural feature where fully functional proteins lack a three-dimensional structure in solution. In this work, we estimated the relative content of intrinsic protein disorder in 96 plant proteomes including monocots and eudicots. In this analysis, we found variation in the relative abundance of intrinsic protein disorder among these major clades; the relative level of disorder is higher in monocots than eudicots. In turn, there is an inverse relationship between the degree of intrinsic protein disorder and protein length, with smaller proteins being more disordered. The relative abundance of amino acids depends on intrinsic disorder and also varies among clades. Within the nucleus, intrinsically disordered proteins are more abundant than ordered proteins. Intrinsically disordered proteins are specialized in regulatory functions, nucleic acid binding, RNA processing, and in response to environmental stimuli. The implications of this on plants’ responses to their environment are discussed.     

Melatonin in the multi‐oscillatory mammalian circadian world

In mammals, the complex interaction of neural, hormonal, and behavioral outputs from the suprachiasmatic nucleus (SCN) drives circadian expression of events, either directly or through coordination of the timing of peripheral oscillators. Melatonin, one of the endocrine output signals of the clock, provides the organism with circadian information and can be considered as an endogenous synchronizer, able to stabilize and reinforce circadian rhythms and to maintain their mutual phase‐relationship at the different levels of the circadian network. Moreover, exogenous melatonin, through an action on the circadian clock, affects all levels of the circadian network. The molecular mechanisms underlying this chronobiotic effect have also been investigated in rats. REV‐ERB α seems to be the initial molecular target.     

Treatment of donor cells with trichostatin A improves in vitro development and reprogramming of buffalo (Bubalus bubalis) nucleus transfer embryos

It has been reported that buffalo (Bubalus bubalis) embryos reconstructed by somatic cell nucleus transfer (SCNT) can develop to the full term of gestation and result in newborn calves. However, the developmental competence of reconstructed embryos is still low. Recently, it has been reported that treating donor cells or embryos with trichostatin A (TSA) can increase the cloning efficiency in some species. Thus, the present study was undertaken to improve the development of buffalo SCNT embryos by treatment of donor cells (buffalo fetal fibroblasts) with TSA and explore the relation between histone acetylation status of donor cells and developmental competence of SCNT embryos. Treatment of donor cells with either 0.15 or 0.3 μM TSA for 48 hours resulted in a significant increase in the cleavage rate and blastocyst yield of SCNT embryos (P < 0.05). Meanwhile, the expression level of HDAC1 in donor cells was also decreased (0.4–0.6 fold, P < 0.05) by TSA treatment, although the expression level of HAT1 was not affected. Further measurement of the epigenetic maker AcH4K8 in buffalo IVF and SCNT embryos at the eight-cell stage revealed that the spatial distribution of acH4K8 staining in SCNT embryos was different from the IVF embryos. Treatment of donor cells with TSA resulted in an increase in the AcH4K8 level of SCNT embryos and similar to fertilized counterparts. These results suggest that treatment of donor cells with TSA can facilitate their nucleus reprogramming by affecting the acetylated status of H4K8 and improving the in vitro development of buffalo SCNT embryos. The AcH4K8 status at the eight-cell stage can be used as an epigenetic marker for predicting the SCNT efficiency in buffalos.     

Organelle aging:Lessons from model organisms

Most cellular processes descend into failure during aging. While a large collection of longevity pathways has been identified in the past decades, the mechanism for age-related decline of cellular homeostasis and organelle function remains largely unsolved. It is known that many organelles undergo structural and functional changes during normal aging, which significantly contributes to the decline of tissue function at old ages. Since recent studies have revealed an emerging role of organelles as regulatory hubs in maintaining cellular homeostasis, understanding of organelle aging will provide important insights into the cellular basis of organismal aging. Here we review current progress on the characterization of age-dependent structural and functional alterations in the more well-studied organelles, as well as the known mechanisms governing organelle aging in model organisms, with a special focus on the fruit fly Drosophila melanogaster.     

孤束核内大剂量注射地塞米松快速引起心血管活动降低

分别将不同剂量的地塞米松注射到大鼠内侧和中间内侧孤束核,观察心血管活动的变化．结果发现：小剂量地塞米松（20或50ng）对心血管活动无明显的影响（P＞0．05）,大剂量地塞米松（100或250ng）注射后10分钟内能使心血管活动明显降低（100ng：－1．80±0．32kPa,－31±13b．／min;250ng：－2．68±0．51kPa,－44±15b．／min;P＜0．01）。不仅如此,小剂量地塞米松（20ng）注入孤束核后对血清中亚硝酸根离子浓度无明显的影响（P＞005）,大剂量地塞米松（250ng）可使血清中亚硝酸根离子浓度显著升高（19．33±0．29μmol／L,vs．control8.26±0.26μmol／L,P＜0.05）。这些结果提示大剂量地塞米松在孤束核内可能通过非基因调控机制捉进外周一氧化氮的形成达到调节心血管活动的作用。     

猫基底前脑胆碱能皮质投射神经元区的P物质样免疫反应神经元

应用免疫组织化学和邻位切片法,研究了猫基底前脑胆碱能皮质投射神经元区的Ｐ物质样免疫反应神经元的分布特征,及其与胆碱乙酰化酶样免疫反应神经元的分布关系,从内侧隔核至Ｍｅｙｎｅｒｔ基底核,２种神经元分布范围相近,且形态,大小相似。但在邻位切片,未见分别呈此二免疫反应的同一神经元的对应剖面。Ｐ物质样免疫反应神经元在内侧隔核和斜角带核数量较多,但在基底核明显减少,在Ｃｈ４间质部及腹侧苍白球连合下部仅为偶见