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991.
Mountain regions contain extraordinary biodiversity. The environmental heterogeneity and glacial cycles often accelerate speciation and adaptation of montane species, but how these processes influence the genomic differentiation of these species is largely unknown. Using a novel chromosome-level genome and population genomic comparisons, we study allopatric divergence and selection in an iconic bird living in a tropical mountain region in New Guinea, Archbold''s bowerbird (Amblyornis papuensis). Our results show that the two populations inhabiting the eastern and western Central Range became isolated ca 11 800 years ago, probably because the suitable habitats for this cold-tolerating bird decreased when the climate got warmer. Our genomic scans detect that genes in highly divergent genomic regions are over-represented in developmental processes, which is probably associated with the observed differences in body size between the populations. Overall, our results suggest that environmental differences between the eastern and western Central Range probably drive adaptive divergence between them. 相似文献
992.
提前接受光照对小鼠视网膜TH和bFGF表达的影响 总被引:1,自引:0,他引:1
目的在通过手术使小鼠提前睁眼接受光照,并成功诱发近视的基础上,进一步研究TH和bFGF在视网膜中的表达变化,以探讨早产近视的发病机理.方法实验用新生第4d的C57BL/6J小鼠,通过手术分离单侧上、下眼睑,使之提前睁眼并接受正常光照,在第14d检查两眼屈光力,应用RT-PCR和免疫组化方法,检测视网膜中bFGF和TH的表达.结果提前接受光照能诱导形成-9.77±0.09D的相对近视.RT-PCR结果显示提前光照小鼠视网膜TH和bFGFmRNA含量明显减少(t值分别为4.316和12.189,P<0.01).免疫组织化学显示TH免疫阳性反应主要分布在节细胞层、内网层和内核层,bFGF免疫阳性反应主要分布在内网层及其两侧的部分节细胞和内核层细胞,另在内网层和视锥视杆层也有微弱表达.免疫组织化学染色显示提前光照小鼠视网膜中TH和bFGF的表达量明显下降.结论研究表明新生小鼠提前光照后,其视网膜TH和bFGF的表达都明显下降,提示TH和bFGF与早产近视的形成有密切关系. 相似文献
993.
利用人工模拟酸性环境,从定期浇注HCl的土壤中筛选出一株脱氮硫杆菌T1菌株,并对其生长特性以及pH、盐度等理化因素对其脱氮除硫性能的影响进行了研究。结果表明,该菌株最适生长pH为7.02,最适脱氮pH为7.0;培养基中NaCl含量低于1.5%时,其脱氮能力没明显变化;与硫酸盐还原菌混菌培养能将H2S氧化为SO42-,从而明显抑制H2S的产生。在液体静置混菌培养过程中,在培养开始后的24 h内,SO42-生成速率最大(11.21 mg/(L·h)),随后不断降低。该菌不仅适用于不同pH、盐度废水的生物处理,还可以与硫酸盐还原菌混合添加到厌氧消化池中以减少硫化物的形成,从而减轻后者对污水处理系统中的金属设备和管道的腐蚀作用以及硫化氢对大气的污染。 相似文献
994.
Recent work reveals that actin acetylation modification has been linked to different normal and disease processes and the effects associated with metabolic and environmental stressors. Herein, we highlight the effects of calreticulin on actin acetylation and cell injury induced by microwave radiation in human microvascular endothelial cell (HMEC). HMEC injury was induced by high-power microwave of different power density (10, 30, 60, 100 mW/cm2, for 6 min) with or without exogenous recombinant calreticulin. The cell injury was assessed by lactate dehydrogenase (LDH) activity and Cell Counting Kit-8 in culture medium, migration ability, intercellular junction, and cytoskeleton staining in HMEC. Western blotting analysis was used to detected calreticulin expression in cytosol and nucleus and acetylation of globular actin (G-actin). We found that HMEC injury was induced by microwave radiation in a dose-dependent manner. Pretreatment HMEC with calreticulin suppressed microwave radiation-induced LDH leakage and increased cell viability and improved microwave radiation-induced decrease in migration, intercellular junction, and cytoskeleton. Meanwhile, pretreatment HMEC with exogenous calreticulin upregulated the histone acetyltransferase activity and the acetylation level of G-actin and increased the fibrous actin (F-actin)/G-actin ratio. We conclude that exogenous calreticulin protects HMEC against microwave radiation-induced injury through promoting actin acetylation and polymerization. 相似文献
995.
自然保护区在生物多样性保护中起着关键作用,然而也面临外来物种入侵等诸多压力。基于72个已调查国家级自然保护区外来入侵植物数据,重点分析生态环境部发布的四批外来入侵物种名单中已有分布的35种外来入侵植物分布格局及其影响因素。研究发现72个国家级自然保护区平均记录有(7.78±0.47)种外来入侵植物,MaxEnt模型预测结果表明98.69%的国家级自然保护区面临外来植物入侵风险。低纬度地区(8.07±0.73)和中纬度地区(9.64±0.56)国家级自然保护区外来入侵植物数量显著高于高纬度地区(4.53±0.88),且不同类型国家级自然保护区外来入侵植物差异不显著。温度和降雨量是影响外来入侵植物在自然保护区分布的关键因素,且影响不同生活型外来入侵植物分布格局的关键因素不同:温度对一年生草本、藤本和灌木的分布解释量极为显著,保护区建立时间、温度、降雨量和海拔共同影响多年生草本植物在国家级自然保护区的分布。研究结果表明国家级自然保护区外来入侵植物调查与监测还存在很大的空白,未来需要进一步加强自然保护区外来入侵植物研究,并提升外来入侵植物的监管能力。 相似文献
996.
Ian G. Ganley Du H. Lam Junru Wang Xiaojun Ding She Chen Xuejun Jiang 《The Journal of biological chemistry》2009,284(18):12297-12305
Autophagy is a degradative process that recycles long-lived and faulty
cellular components. It is linked to many diseases and is required for normal
development. ULK1, a mammalian serine/threonine protein kinase, plays a key
role in the initial stages of autophagy, though the exact molecular mechanism
is unknown. Here we report identification of a novel protein complex
containing ULK1 and two additional protein factors, FIP200 and ATG13, all of
which are essential for starvation-induced autophagy. Both FIP200 and ATG13
are critical for correct localization of ULK1 to the pre-autophagosome and
stability of ULK1 protein. Additionally, we demonstrate by using both cellular
experiments and a de novo in vitro reconstituted reaction that FIP200
and ATG13 can enhance ULK1 kinase activity individually but both are required
for maximal stimulation. Further, we show that ATG13 and ULK1 are
phosphorylated by the mTOR pathway in a nutrient starvation-regulated manner,
indicating that the ULK1·ATG13·FIP200 complex acts as a node for
integrating incoming autophagy signals into autophagosome biogenesis.Macroautophagy (herein referred to as autophagy) is a catabolic process
whereby long-lived proteins and damaged organelles are shuttled to lysosomes
for degradation. This process is conserved in all eukaryotes. Under normal
growth conditions a housekeeping level of autophagy exists. Under stress, such
as nutrient starvation, autophagy is strongly induced resulting in the
engulfment of cytosolic components and organelles in specialized
double-membrane structures termed autophagosomes. Following fusion of the
outer autophagosomal membrane with lysosomes, the inner membrane and its
cytoplasmic cargo are degraded and recycled
(1–3).
Recent work has implicated autophagy in many disease pathologies, including
cancer, neurodegeneration, as well as in eliminating intracellular pathogens
(4–8).The morphology of autophagy was first described in mammalian cells over 50
years ago (9). However, it is
only recently through yeast genetic screens, that multiple autophagy-related
(ATG) genes have been identified
(10–12).
The yeast ATG proteins have been classified into four major groups: the Atg1
protein kinase complex, the Vps34 phosphatidylinositol 3-phosphate kinase
complex, the Atg8/Atg12 conjugation systems, and the Atg9 recycling complex
(13). Even though many ATG
genes are now known, most of which have functional homologs in mammalian cells
(14,
15), the molecular mechanism
by which they sense the initial triggers and subsequently dictate
autophagy-specific intracellular membrane events is far from understood.In yeast, one of the earliest autophagy-specific events is believed to
involve the Atg1 protein kinase complex. Atg1 is a serine/threonine protein
kinase and a key autophagy-regulator
(16). Atg1 is complexed to at
least two other proteins during autophagy, Atg13 and Atg17, both of which are
required for normal Atg1 function and autophagosome generation
(17–19).
Classical signaling pathways such as the cAMP-dependent kinase (PKA) pathway
or the Tor kinase pathway appear to converge upon this complex, placing Atg1
at an early stage during autophagosome biogenesis
(20–22).
Atg1 phosphorylation by PKA blocks its association with the forming
autophagosome (21), while the
Tor pathway hyperphosphorylates Atg13 causing a reduced affinity of Atg13 for
Atg1, resulting in repression of autophagy
(17,
19). In contrast, nutrient
starvation or inhibition of Tor leads to dephosphorylation of Atg13 thus
increased Atg1 complex formation and kinase activity, resulting in stimulation
of autophagy (19).
Surprisingly, the physiological substrates of Atg1 kinase have not been
identified; thus how Atg1 transduces upstream autophagic signaling is
undefined. Recently, mammalian homologs of Atg1 have been identified as ULK1
and ULK2 (Unc-51-like
kinase)2
(23–25).
ULK1 and ULK2 are ubiquitously expressed and localize to the isolation
membrane, or forming autophagosome, upon nutrient starvation
(25); RNAi-mediated depletion
of ULK1 in HEK293 cells compromises autophagy
(23,
24). The exact role of ULK1
versus ULK2 in autophagy is unclear, and it is possible some
redundancy exists between the two isoforms
(26).Given the conservation of autophagy from yeast to man, it is interesting to
note that no mammalian counterpart to yeast Atg13 or Atg17 had been identified
until very recently. The protein FIP200 (focal adhesion kinase
family-interacting protein of 200 kDa) was
identified as an autophagy-essential binding partner of both ULK1 and ULK2
(25), and it has been
speculated that FIP200 might be the equivalent of yeast Atg17, despite low
sequence similarity (25,
27).In this study, we delve deeper into the molecular regulation of ULK1 to
gain a better insight into how mammalian signaling pathways affect autophagy
initiation. We describe here the identification of a triple complex consisting
of ULK1, FIP200, and the mammalian equivalent of Atg13. This complex is
required not only for localization of ULK1 to the isolation membrane but also
for maximal kinase activity. In addition, both ATG13 and ULK1 are kinase
substrates in the mTOR pathway and thus might function to sense nutrient
starvation. Therefore, this study defines the role of mammalian
ULK1-ATG13-FIP200 complex in mediating the initial autophagic triggers and to
transduce the signal to the core autophagic machinery. 相似文献
997.
Lateral hypothalamic Orexin‐A‐ergic projections to the arcuate nucleus modulate gastric function in vivo 下载免费PDF全文
Xiao Luan Xiangrong Sun Feifei Guo Di Zhang Cheng Wang Li Ma Luo Xu 《Journal of neurochemistry》2017,143(6):697-707
998.
为探究外来入侵植物豚草(Ambrosia artemisiifolia)对本地植物群落结构的影响,结合区内林下草本植物调查和室内分析方法,分析了豚草不同入侵压力下(无入侵、轻度入侵、中度入侵、重度入侵)本地草本植物丰富度、盖度等特征,探讨了地形、气候、土壤、光照、人口密度等外部因素与豚草种群特征、本地植物群落结构之间的关系。结果表明:豚草种群盖度与其高度、密度、生物量显著正相关。与对照相比,轻度入侵下本土草本植物Shannon-Wiener多样性指数和Pielou均匀度指数显著增加,丰富度、盖度未出现显著差异。随着豚草入侵程度加剧,本地草本植物物种丰富度、盖度极显著降低,样方Shannon-Wiener多样性指数先升高再降低,本土草本植物Pielou均匀度指数差异不显著。冗余分析(RDA)表明,土壤全氮、与道路距离、土壤全磷、郁闭度对研究区植物群落结构影响最大,土壤全氮含量随豚草盖度和生物量增加而减少,距道路越近或光照越强,豚草盖度和生物量越高。增强伊犁河谷地区交通往来货物豚草检验检疫力度、增加林内植被郁闭度或是抑制区内豚草入侵的有效手段。 相似文献
999.
The involvement of nitric oxide in ultraviolet-B-inhibited pollen germination and tube growth of Paulownia tomentosa in vitro 总被引:1,自引:0,他引:1
The role of nitric oxide (NO) in the ultraviolet-B radiation (UV-B)-induced reduction of in vitro pollen germination and tube growth of Paulownia tomentosa Steud. was studied. Results showed that exposure of the pollen to 0.4 and 0.8 W m−2 UV-B radiation for 2 h resulted in not only the reduction of pollen germination and tube growth but also the enhancement of NO synthase (NOS, EC 1.14.13.39) activity and NO production in pollen grain and tube. Also, exogenous NO donors sodium nitroprusside and S -nitrosoglutathione inhibited both pollen germination and tube growth in a dose-dependence manner. NOS inhibitor NG -nitro- l -Arg-methyl eater ( l -NAME) and NO scavenger 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (c-PTIO) not only largely prevented the NO generation but also partly reversed the UV-B-inhibited pollen germination and tube growth. These results indicate that UV-B radiation inhibits pollen germination and tube growth partly via promoting NO production in pollen grain and tube by a NOS-like enzyme. Additionally, a guanylyl cyclase inhibitor 6-anilino-5,8-quinolinequinone (LY-83583) prevented both the UV-B- and NO donors-inhibited pollen germination and tube growth, suggesting that the NO function is mediated by cyclic guanosine 5'-monophosphate. However, the effects of c-PTIO, l -NAME and LY-83583 on the UV-B-inhibited pollen germination and tube growth were only partial, suggesting that there are NO-independent pathways in UV-B signal networks. 相似文献
1000.