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1,092 result(s) for "Rea, L"
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Temperature-dependent growth contributes to long-term cold sensing
Temperature is a key factor in the growth and development of all organisms 1 , 2 . Plants have to interpret temperature fluctuations, over hourly to monthly timescales, to align their growth and development with the seasons. Much is known about how plants respond to acute thermal stresses 3 , 4 , but the mechanisms that integrate long-term temperature exposure remain unknown. The slow, winter-long upregulation of VERNALIZATION INSENSITIVE 3 (VIN3) 5 – 7 , a PHD protein that functions with Polycomb repressive complex 2 to epigenetically silence FLOWERING LOCUS C ( FLC ) during vernalization, is central to plants interpreting winter progression 5 , 6 , 8 – 11 . Here, by a forward genetic screen, we identify two dominant mutations of the transcription factor NTL8 that constitutively activate VIN3 expression and alter the slow VIN3 cold induction profile. In the wild type, the NTL8 protein accumulates slowly in the cold, and directly upregulates VIN3 transcription. Through combining computational simulation and experimental validation, we show that a major contributor to this slow accumulation is reduced NTL8 dilution due to slow growth at low temperatures. Temperature-dependent growth is thus exploited through protein dilution to provide the long-term thermosensory information for VIN3 upregulation. Indirect mechanisms involving temperature-dependent growth, in addition to direct thermosensing, may be widely relevant in long-term biological sensing of naturally fluctuating temperatures. The authors find that slow plant growth at low temperatures during winter reduces dilution of the transcription factor NTL8, which allows slow accumulation of NTL8 and thus the gradual increase in transcription of VIN3 —a gene involved in memory of cold exposure.
رينكيتينك في أوز
هذه الرواية هي تسجيل أمين للمهمة المحفوفة بالمخاطر التي خاضها الأمير إنجا والملك رينكيتينك والكبش بلبل لتحرير شعب جزيرة بينجاري، التي تقع خارج حدود أرض أوز في المحيط الواسع الكبير نونيستك ؛ ما قصة اللآلئ الثلاث السحرية ؟ ولكن كيف انتهى الحال بوالدي الأمير أسرى في قبضة ملك النوم ؟ وكيف استطاع الأمير تحريرهم ؟ هذا ما ستعرفه في هذه الرواية العاشرة التي ستنتهي في أرض أوز.
Absence of warmth permits epigenetic memory of winter in Arabidopsis
Plants integrate widely fluctuating temperatures to monitor seasonal progression. Here, we investigate the temperature signals in field conditions that result in vernalisation, the mechanism by which flowering is aligned with spring. We find that multiple, distinct aspects of the temperature profile contribute to vernalisation. In autumn, transient cold temperatures promote transcriptional shutdown of Arabidopsis FLOWERING LOCUS C ( FLC ), independently of factors conferring epigenetic memory. As winter continues, expression of VERNALIZATION INSENSITIVE3 (VIN3), a factor needed for epigenetic silencing, is upregulated by at least two independent thermosensory processes. One integrates long-term cold temperatures, while the other requires the absence of daily temperatures above 15 °C. The lack of spikes of high temperature, not just prolonged cold, is thus the major driver for vernalisation. Monitoring of peak daily temperature is an effective mechanism to judge seasonal progression, but is likely to have deleterious consequences for vernalisation as the climate becomes more variable. Plants use multiple cues to monitor seasonal temperatures. Here, the authors show that Arabidopsis requires not only prolonged cold, but the absence of temperature spikes above 15 °C to epigenetically silence FLC during winter.
الطريق إلى أوز
رواية ساحر أوز العجيب تأليف ليمان فرانك بام، ترجمة طه عبد المنعم .. هذه الرواية من الأعمال الكلاسيكية الرائدة في الأدب الأمريكي، ونشرت لأول مرة في بدايات القرن العشرين، ثم تبعها المؤلف بسلسلة طويلة انتهت في منتصف القرن الماضي. تدور أحداث الرواية حول فتاة صغيرة اسمها دوروثي، تعيش مع عمّاتها في مزرعة صغيرة في كانساس.
Relationship Between Mitochondrial Electron Transport Chain Dysfunction, Development, and Life Extension in Caenorhabditis elegans
Prior studies have shown that disruption of mitochondrial electron transport chain (ETC) function in the nematode Caenorhabditis elegans can result in life extension. Counter to these findings, many mutations that disrupt ETC function in humans are known to be pathologically life-shortening. In this study, we have undertaken the first formal investigation of the role of partial mitochondrial ETC inhibition and its contribution to the life-extension phenotype of C. elegans. We have developed a novel RNA interference (RNAi) dilution strategy to incrementally reduce the expression level of five genes encoding mitochondrial proteins in C. elegans: atp-3, nuo-2, isp-1, cco-1, and frataxin (frh-1). We observed that each RNAi treatment led to marked alterations in multiple ETC components. Using this dilution technique, we observed a consistent, three-phase lifespan response to increasingly greater inhibition by RNAi: at low levels of inhibition, there was no response, then as inhibition increased, lifespan responded by monotonically lengthening. Finally, at the highest levels of RNAi inhibition, lifespan began to shorten. Indirect measurements of whole-animal oxidative stress showed no correlation with life extension. Instead, larval development, fertility, and adult size all became coordinately affected at the same point at which lifespan began to increase. We show that a specific signal, initiated during the L3/L4 larval stage of development, is sufficient for initiating mitochondrial dysfunction-dependent life extension in C. elegans. This stage of development is characterized by the last somatic cell divisions normally undertaken by C. elegans and also by massive mitochondrial DNA expansion. The coordinate effects of mitochondrial dysfunction on several cell cycle-dependent phenotypes, coupled with recent findings directly linking cell cycle progression with mitochondrial activity in C. elegans, lead us to propose that cell cycle checkpoint control plays a key role in specifying longevity of mitochondrial mutants.
تيك توك في أوز
من أجواء الرواية الثامنة في عالم أوز، عن مغامرة المتشرد للبحث عن شقيقه المحبوس عند ملك النوم. ترافقه بيتسي بوبيان ، التي تصل الأراضي الخيالية بعد تحطم سفينتها في عرض البحر مع البغل هانك، وبوليكروم ابنة قوس قزح، والأميرة أورج، الأميرة المنفية من مملكة الورد. بيتسي بوبيان ستكون رفيقة دورثي في مغامراتها القادمة، ومملكة النوم ستحدث فيها تغيرات هائلة، وبالطبع ستلاحظون قصة الحب بين الجندي جو كتب والأميرة أورج، ولم يبخل علينا المؤرخ الملكي لأرض أوز بالمزيد من المغامرات المثيرة للاقتحام وغزو مملكة النوم وإنقاذ شقيق المتشرد.
Feeling Every Bit of Winter – Distributed Temperature Sensitivity in Vernalization
Temperature intrinsically influences all aspects of biochemical and biophysical processes. Organisms have therefore evolved strategies to buffer themselves against thermal perturbations. Many organisms also use temperature signals as cues to align behavior and development with certain seasons. These developmentally important thermosensory mechanisms have generally been studied in constant temperature conditions. However, environmental temperature is an inherently noisy signal, and it has been unclear how organisms reliably extract specific temperature cues from fluctuating temperature profiles. In this context, we discuss plant thermosensory responses, focusing on temperature sensing throughout vernalization in Arabidopsis. We highlight many different timescales of sensing, which has led to the proposal of a distributed thermosensing paradigm. Within this paradigm, we suggest a classification system for thermosensors. Finally, we focus on the longest timescale, which is most important for sensing winter, and examine the different mechanisms in which memory of cold exposure can be achieved.
خيال المآته في أوز
تقود المغامرات كابتن بيل، البحار العجوز ذا الساق الخشبية، وتروت، الفتاة الصغيرة- إلى مملكة معزولة ومنسية داخل أرض أوز. وهناك يشهدون مؤامرات لئيمة لإفساد قصة حب بين الأميرة وصبي البستاني، ولكنهم يقعون في مزيد من المشاكل والمؤامرات، حتى يحضر بطل أرض أوز، خيال المآتة. ولكن هل يستطيع رجل القش إنقاذ الموقف المعقد الذي وقع أبطالنا فيه؟ ومواجهة السحر الأسود والمرعب للساحرة بلينكي؟ دعنا نستكشف الرواية التاسعة من عالم أوز!.
p62 overexpression induces TDP-43 cytoplasmic mislocalisation, aggregation and cleavage and neuronal death
Amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD) that exist on a spectrum of neurodegenerative disease. A hallmark of pathology is cytoplasmic TDP-43 aggregates within neurons, observed in 97% of ALS cases and ~ 50% of FTLD cases. This mislocalisation from the nucleus into the cytoplasm and TDP-43 cleavage are associated with pathology, however, the drivers of these changes are unknown. p62 is invariably also present within these aggregates. We show that p62 overexpression causes TDP-43 mislocalisation into cytoplasmic aggregates, and aberrant TDP-43 cleavage that was dependent on both the PB1 and ubiquitin-associated (UBA) domains of p62. We further show that p62 overexpression induces neuron death. We found that stressors (proteasome inhibition and arsenic) increased p62 expression and that this shifted the nuclear:cytoplasmic TDP-43 ratio. Overall, our study suggests that environmental factors that increase p62 may thereby contribute to TDP-43 pathology in ALS and FTLD.