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棉花全生育期叶片SPAD值的遥感估算模型
Remote sensing estimation model of cotton leaf SPAD value at the whole growth period
 [PDF]

马文君,常庆瑞,田明璐,班松涛
- , 2017, DOI: 10.7606/j.issn.1000-7601.2017.05.07
Abstract: 叶绿素含量是评估棉花生长状况的重要参数,估算叶绿素含量对于棉花生长监测具有重要意义。以渭北旱塬区种植的棉花为试验材料,测量全生育期棉花叶片SPAD值与冠层反射率光谱,将原始高光谱反射率、一阶微分光谱反射率、不同波段组合的遥感光谱参数分别与SPAD值做相关性分析,用传统回归分析方法构建五种重要光谱参数的SPAD值预测模型,同时,采用PLSR方法建立全生育期SPAD值的估算模型。最后对模型进行检验,筛选出精度最高的模型。建模结果表明,基于多种光谱参数的全生育期PLSR预测模型精度最高、预测效果最好,估算模型的决定系数R2为0.733,验证模型R2为0.737。PLSR方法建立的多光谱参数的SPAD值估算模型预测效果显著,利用高光谱技术对棉花SPAD值进行监测,可为全生育期棉花长势遥感监测提供依据。
Chlorophyll concentration is an important parameter to evaluate cotton’s growth conditions. So it is significant to estimate chlorophyll content for monitoring of cotton growth information. The materials of this research was the cotton in field in Wei-bei plateau region. Firstly the SPAD value was measured with SPAD-502 in field, and the spectral reflectance of canopy was measured with SVC Handheld spectrometer. Then the correlation was analyzed between the SPAD value and single narrow band raw reflectance, or the first derivative spectral reflectance, or spectral indices combined from different band. The prediction model was established with 5 representative spectral indices. At the same time, the simulation model of remote sensing of canopy SPAD value at the whole growth period in cotton was estimated based on PLSR method. Finally, the highest precision model was filtered out by testing. The result showed that the model based on various spectral indices with PLSR method obtained the most satisfing results for the estimation of chlorophyll concentration, R2 of the estimation model is 0.733, R2 of the verification model was up to 0.737. The remote sensing models at the whole growth stage in cotton built with PLSR method based on important spectral indices provides a basis for monitoring cotton crop growing trend and forecasting production with reliable forecast.
Chilling Stress—The Key Predisposing Factor for Causing Alternaria alternata Infection and Leading to Cotton (Gossypium hirsutum L.) Leaf Senescence  [PDF]
Jingqing Zhao, Sha Li, Tengfei Jiang, Zhi Liu, Wenwei Zhang, Guiliang Jian, Fangjun Qi
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0036126
Abstract: Leaf senescence plays a vital role in nutrient recycling and overall capacity to assimilate carbon dioxide. Cotton premature leaf senescence, often accompanied with unexpected short-term low temperature, has been occurring with an increasing frequency in many cotton-growing areas and causes serious reduction in yield and quality of cotton. The key factors for causing and promoting cotton premature leaf senescence are still unclear. In this case, the relationship between the pre-chilling stress and Alternaria alternata infection for causing cotton leaf senescence was investigated under precisely controlled laboratory conditions with four to five leaves stage cotton plants. The results showed short-term chilling stress could cause a certain degree of physiological impairment to cotton leaves, which could be recovered to normal levels in 2–4 days when the chilling stresses were removed. When these chilling stress injured leaves were further inoculated with A. alternata, the pronounced appearance and development of leaf spot disease, and eventually the pronounced symptoms of leaf senescence, occurred on these cotton leaves. The onset of cotton leaf senescence at this condition was also reflected in various physiological indexes such as irreversible increase in malondialdehyde (MDA) content and electrolyte leakage, irreversible decrease in soluble protein content and chlorophyll content, and irreversible damage in leaves' photosynthesis ability. The presented results demonstrated that chilling stress acted as the key predisposing factor for causing A. alternata infection and leading to cotton leaf senescence. It could be expected that the understanding of the key factors causing and promoting cotton leaf senescence would be helpful for taking appropriate management steps to prevent cotton premature leaf senescence.
Autophagy Impairment Induces Premature Senescence in Primary Human Fibroblasts  [PDF]
Hyun Tae Kang,Ki Baek Lee,Sung Young Kim,Hae Ri Choi,Sang Chul Park
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0023367
Abstract: Recent studies have demonstrated that activation of autophagy increases the lifespan of organisms from yeast to flies. In contrast to the lifespan extension effect in lower organisms, it has been reported that overexpression of unc-51-like kinase 3 (ULK3), the mammalian homolog of autophagy-specific gene 1 (ATG1), induces premature senescence in human fibroblasts. Therefore, we assessed whether the activation of autophagy would genuinely induce premature senescence in human cells.
Identification of genes associated with cotyledon senescence in upland cotton
Fafu Shen,Shuxun Yu,Qingen Xie,Xiulan Han,Shuli Fan
Chinese Science Bulletin , 2006, DOI: 10.1007/s11434-006-1085-5
Abstract: In order to unravel the biochemical pathways and understand the molecular mechanisms involved in leaf senescence, suppression subtractive hybridization (SSH) was used to generate a cDNA library enriched for transcripts differentially expressed in developmental senescence cotyledons of upland cotton. After differential screening by membrane-based hybridization and subsequent confirmation by reverse Northern blot analysis, selected 678 clones were sequenced and analyzed. Sequencing of these cDNA fragments reveals that 216 of expressed sequence tags (ESTs) represented unique genes. Of these 216 cDNAs, 151 clones (69.9%) show significant homologies to previously known genes, while the remaining 65 do not match any known sequences. 151 unique ESTs are assigned to twelve different categories based on their putative functions generated by BLAST analysis. These SAG-encoded proteins are likely to participate in macromolecule degradation, nutrient recycling, detoxification of oxidative metabolites, and signaling and regulatory events. The expression pattern of selection of genes was confirmed using northern hybridization. Northern hybridization confirmed several distinct patterns, from expression at a very early stage to the terminal phase of the senescence syndrome. Clones encoding proteases and proteins involved in macromolecule degradation and gluconeogenesis, as well as stress-related genes, are up regulated in senescence cotyledons.
Identification of genes associated with cotyledon senescence in upland cotton
Fafu Shen,Shuxun Yu,Qingen Xie,Xiulan Han,Shuli Fan,
SHEN
,Fafu,YU,Shuxun,XlE,Qingen,HAN,Xiulan,FAN,Shuli

科学通报(英文版) , 2006,
Abstract: Leaf senescence in plants is an essential develop- mental phase, and an understanding of senescence is important not only for pure scientific reasons, but also for practical purposes. During the last decade, a number of senescence-associated genes (SAGs) …
Role of in Replicative Senescence and DNA Damage-Induced Premature Senescence in p53-Deficient Human Cells  [PDF]
Razmik Mirzayans,Bonnie Andrais,Gavin Hansen,David Murray
Biochemistry Research International , 2012, DOI: 10.1155/2012/951574
Abstract: The p16INK4A (hereafter p16) tumor suppressor is encoded by the INK4A/ARF locus which is among the most commonly dysregulated sequences in human cancer. By inhibiting cyclin-dependent kinases, p16 activates the G1-S checkpoint, and this response is often considered to be critical for establishing a senescence-like growth arrest. Not all studies support a universal role for p16 in senescence. Single-cell analysis of noncancerous human fibroblast cultures undergoing senescence as a function of culture age (replicative senescence) has revealed that p16 is not expressed in the majority (>90%) of cells that exhibit features of senescence (e.g., flattened and enlarged morphology coupled with senescence-associated β-galactosidase expression), ruling out a requirement for p16 in this process. In addition, ionizing radiation triggers premature senescence in human cancer cell lines that do not express p16. These observations are made with cells that express wild-type p53, a key mediator of the DNA damage response. In this paper, we examine the growing evidence suggesting a negative regulatory relationship between p16 and p53 and discuss recent reports that implicate a role for p16 in replicative senescence and ionizing radiation-induced premature senescence in human cells that lack wild-type p53 function.
Role of in Replicative Senescence and DNA Damage-Induced Premature Senescence in p53-Deficient Human Cells  [PDF]
Razmik Mirzayans,Bonnie Andrais,Gavin Hansen,David Murray
Biochemistry Research International , 2012, DOI: 10.1155/2012/951574
Abstract: The (hereafter p16) tumor suppressor is encoded by the INK4A/ARF locus which is among the most commonly dysregulated sequences in human cancer. By inhibiting cyclin-dependent kinases, p16 activates the G1-S checkpoint, and this response is often considered to be critical for establishing a senescence-like growth arrest. Not all studies support a universal role for p16 in senescence. Single-cell analysis of noncancerous human fibroblast cultures undergoing senescence as a function of culture age (replicative senescence) has revealed that p16 is not expressed in the majority (>90%) of cells that exhibit features of senescence (e.g., flattened and enlarged morphology coupled with senescence-associated β-galactosidase expression), ruling out a requirement for p16 in this process. In addition, ionizing radiation triggers premature senescence in human cancer cell lines that do not express p16. These observations are made with cells that express wild-type p53, a key mediator of the DNA damage response. In this paper, we examine the growing evidence suggesting a negative regulatory relationship between p16 and p53 and discuss recent reports that implicate a role for p16 in replicative senescence and ionizing radiation-induced premature senescence in human cells that lack wild-type p53 function. 1. Introduction Normal somatic human cells in culture undergo a finite number of divisions before entering a state of irreversible growth arrest termed ‘‘replicative senescence” [1]. This phenotype is characterized by the acquisition of flattened and enlarged cell morphology, presence of β-galactosidase activity at suboptimal conditions (i.e., pH 6), and absence of cell division in metabolically active cells. Replicative senescence is triggered by erosion and dysfunction of telomeres and is mediated by multibranched signaling processes [2, 3]. Exposure of certain immortalized cell types (e.g., p53-proficient human solid tumor-derived cell lines), as well as “young” (early-passage) normal human cells (e.g., skin fibroblasts) to DNA-damaging agents can also trigger a state of sustained growth arrest resembling senescence. The DNA damage-triggered response is commonly called “stress-induced premature senescence” (SIPS). Unlike replicative senescence, SIPS is independent of telomere length or function [3]. Bypassing replicative senescence is a prerequisite step in immortalization and malignant transformation [4], and escape from SIPS can lead to the emergence of highly metastatic and therapy-resistant cells [5, 6]. Accordingly, a great deal of research has been directed
Predicting nitrogen fertilization using spad index for cotton in semi-arid region
Ziany Neiva Brand?o,Valdinei Sofiatti,Gilvan Barbosa Ferreira,Rosiane de Lourdes Silva de Lima
Engenharia Ambiental : Pesquisa e Tecnologia , 2009,
Abstract: Accurate assessments of leaf nitrogen content are needed to ensure high productivity in crop management and prevent environmental damages. However, laboratory methods of quantifying N content are costly and time consuming. The objective of this study was to evaluate the accuracy of the Minolta SPAD-502 readings for early assessing of leaf N content and cotton yield, providing subsidies for real-time recommendation of nitrogen fertilization. It was used a randomized block design with 3 replications. The treatments were arranged in a split-plot in time, where was evaluated the effects of four N doses, (0, 90, 180 and 270 kg ha-1) into plots, and the effects of four evaluation seasons, (40, 60, 80, 100 DAE) in the subplots. Were done assessments when was determined the leaf nitrogen content and the SPAD index during the evaluation seasons and at the harvest the yield. The readings of the SPAD-502 allowed figure out mathematical models for predicting the content of N in cotton leaves in a simple way and with high precision. It’s possible to correct the crop nitrogen deficiency and restore partially or totally the yield, using nitrogen supplementation rates obtained with SPAD index from 40 until 90 days after emergence applied by fertirigation. Keywords: Gossypium hirsutum, mineral nutrition, nitrous oxide, environmental damages, yield
A Micro-RNA Connection in -Mediated Premature Senescence of Human Melanocytes  [PDF]
Gang Ren,Jingwei Feng,Ila Datar,Aaron H. Yeung,Srinivas Vinod Saladi,Yongqing Feng,Ivana de la Serna,Kam C. Yeung
International Journal of Cell Biology , 2012, DOI: 10.1155/2012/913242
Abstract: Recent high-throughput-sequencing of the cancer genome has identified oncogenic mutations in BRaf genetic locus as one of the critical events in melanomagenesis. In normal cells, the activity of BRaf is tightly regulated. Gain-of-function mutations like those identified in melanoma frequently lead to enhanced cell-survival and unrestrained growth. The activating mutation of BRaf will also induce the cells to senesce. However, the mechanism by which the oncogenic BRaf induces the senescent barrier remains poorly defined. microRNAs have regulatory functions toward the expression of genes that are important in carcinogenesis. Here we show that expression of several microRNAs is altered when the oncogenic version of BRaf is introduced in cultured primary melanocytes and these cells undergo premature cellular senescence. These include eight microRNAs whose expression rates are significantly stimulated and three that are repressed. While most of the induced microRNAs have documented negative effects on cell cycle progression, one of the repressed microRNAs has proven oncogenic functions. Ectopic expression of some of these induced microRNAs increased the expression of senescence markers and induced growth arrest and senescence in primary melanocytes. Taken together, our results suggest that the change in microRNA expression rates may play a vital role in senescence induced by the oncogenic BRaf. 1. Introduction Unregulated oncogene expression during cancer development causes cancer cells to senesce prematurely, a gene-directed program that irrevocably induces cell cycle arrest [1–4]. First described in cell culture [5], oncogene-induced senescence (OIS) has been confirmed in vivo as a vital mechanism that constrains the malignant progression of many tumors [3]. Unregulated oncoproteins promote senescence by activating effector pathways that are cell-type and oncogene specific. Recent progress identified different regulatory circuitries of OIS, but much remains to be learned [6]. High-throughput sequencing of the cancer genomes has identified BRaf kinase as the most frequently mutated (50–70%) oncogene in melanoma [7]. About 90% of BRaf gain-of-function mutations are at position 600 with glutamic acid (E) inserted for valine (V) [7]. BRaf is a serine/threonine protein kinase that functions directly downstream of the small GTPase Ras and upstream of the MEK and ERK mitogen-activated protein kinase (MAPK) cascade. This mutation significantly increases BRaf kinase activity toward MEK, causing constitutive BRaf-MEK-ERK signaling [7, 8]. The BRaf gain-of-function
Premature Senescence and Increased TGFβ Signaling in the Absence of Tgif1  [PDF]
Brad J. Zerlanko, Laurent Bartholin, Tiffany A. Melhuish, David Wotton
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0035460
Abstract: Transforming growth factor β (TGFβ) signaling regulates cell cycle progression in several cell types, primarily by inducing a G1 cell cycle arrest. Tgif1 is a transcriptional corepressor that limits TGFβ responsive gene expression. Here we demonstrate that primary mouse embryo fibroblasts (MEFs) lacking Tgif1 proliferate slowly, accumulate increased levels of DNA damage, and senesce prematurely. We also provide evidence that the effects of loss of Tgif1 on proliferation and senescence are not limited to primary cells. The increased DNA damage in Tgif1 null MEFs can be partially reversed by culturing cells at physiological oxygen levels, and growth in normoxic conditions also partially rescues the proliferation defect, suggesting that in the absence of Tgif1 primary MEFs are less able to cope with elevated levels of oxidative stress. Additionally, we show that Tgif1 null MEFs are more sensitive to TGFβ-mediated growth inhibition, and that treatment with a TGFβ receptor kinase inhibitor increases proliferation of Tgif1 null MEFs. Conversely, persistent treatment of wild type cells with low levels of TGFβ slows proliferation and induces senescence, suggesting that TGFβ signaling also contributes to cellular senescence. We suggest that in the absence of Tgif1, a persistent increase in TGFβ responsive transcription and a reduced ability to deal with hyperoxic stress result in premature senescence in primary MEFs.
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