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PubMed2006

Tgf-Beta pathway as a potential target in neurodegeneration and Alzheimer's.

Alzheimer's disease (AD) is a fatal neurodegenerative disease characterized by the loss of large numbers of forebrain neurons. There are currently no effective AD treatments available and the cause of the disease is unknown in the majority of cases. Because normal neuronal maintenance and survival depends on stimulation of key signaling pathways by a number of neurotrophic factors it has been postulated that reduced signaling by or expression of these factors may promote neurodegeneration. Growing evidence suggests that the transforming growth factor-beta (TGF-beta) signaling pathway may be one such neurotrophic pathway that meets important protective and survival roles in neurons. Here I explore this evidence and discuss the pathway as a potential target for the treatment of neurodegeneration and AD.

Alzheimer Disease↗
PubMed1996

Integrin-dependent signal transduction.

Integrins are receptor molecules for extracellular matrix molecules (e.g., the beta(1) family), serum components (alpha(v) family) and immunoglobulin family adhesion molecules (beta(2) family). Integrin-dependent adhesion has also been shown to have metabolic consequences. Adhesion to a variety of extracellular matrix proteins, such as fibronectin, collagen, and laminin, is a potent regulator of cell growth, differentiation, and gene expression. Ligand binding or aggregation of integrin receptors initiates a number of metabolic changes including activation of serine/threonine and tyrosine kinases, increased Ca2+ influx, increased cytoplasmic alkalinization, and altered inositol lipid metabolism. In some instances activation of transcription factors and induction of gene expression have also been demonstrated. Components of key signaling pathways involving integrins are beginning to be identified. Some studies have shown that integrins form multi-component complexes with signal transduction molecules. Elucidating the interactions of the signal transduction molecules with each other and with the integrin cytoplasmic domains will be key to understanding the initial events of signal transduction through the integrins.

Animals↗
PubMed2001

Role of the oncogenic Raf-1 in orchestration of discrete nuclear factor-kappaB-activating pathways.

Raf-1, a key kinase in the Ras signaling pathway, plays critical roles in cell differentiation, proliferation, and tumorigenesis. However, knowledge of the Raf-1 in inflammation is limited. Using an inducible oncogenic Raf-1, we show that the Raf-1 orchestrates the discrete NF-kappaB activating pathways. While the Raf-1 activation induces a modest IkappaB degradation by enhancing the basal IkappaB kinase activity, it contradictorily suppresses the proinflammatory cytokine inducible IkappaB kinase complex, leading to an inhibition of TNF-alpha- and IL-1beta-induced NF-kappaB activation. Despite considerable degrees of overlap, LPS signaling is not affected by Raf-1. By either conditionally reducing Raf-1 activity or completely disrupting the Raf-1 signaling by PD98059, a specific inhibitor of MEK1, the otherwise inhibited cytokine responses can be restored. Moreover, when the activity of Raf-1 is up-regulated during the cell cycle progression from the G(0) phase to the late G(1) phase, the enhanced Raf-1 activity suffices to shift the TNF-alpha response from the sensitive to the insensitive state. Together, these studies elucidate a mechanism by which signaling outputs are shaped by the intracellular Raf-1, thus explaining the "cellular context"-dependent cytokine response.

Animals↗
PubMed2005

Zebrafish as a model for myelopoiesis during embryogenesis.

Zebrafish produce nearly identical hematopoeitic cell lineages to those found in mammals and other higher vertebrates. As in mammals, blood cell development proceeds in distinct waves, constituting embryonic (primitive) and adult (definitive) hematopoiesis. The conservation of genes such as scl, pu.1, c/ebpalpha, mpo, l-plastin, and lysozyme C in myelopoiesis and the corresponding expression patterns in zebrafish suggests that shared genetic pathways regulate this complex developmental process. In the zebrafish model system, experimental approaches have been applied, including RNA in situ hybridization, morpholino injections, and the analysis of mutant and transgenic fish lines, leading to improved understanding of the regulation in vivo of key molecular pathways with conserved roles in vertebrate myelopoiesis.

Animals↗
PubMed2001

The benefits of using clinical pathways for managing acute paediatric illness in an emergency department.

The aim of this study was to provide an evaluation of the overall effectiveness of using a number of clinical pathways in treating common acute paediatric conditions in an emergency department. This was a before and after study conducted on the effectiveness of three clinical pathways (gastroenteritis, asthma, and croup) in the emergency department of the Children's Hospital at Westmead, conducted over two separate yearly periods January to December 1996 and January to December 1999 representing before and after the introduction of clinical pathways in the emergency department. The main outcomes of the effectiveness of the pathways, namely admission to an in-patient bed, length of hospital stay and re-presentation after discharge from the ED were compared. Other outcomes of interest such as parental satisfaction and patient waiting times were also presented. Any deviation from a key clinical pathway process was reported. A total of 2854 children were managed by a clinical pathway compared to 2680 children managed before clinical pathways were introduced. The admission rate was reduced by threefold (9.1% compared to 23.6%) with a twofold reduction in length of hospital stay (32.7 h compared to 17.5 h). In 3.6% of children using a clinical pathway an unscheduled medical visit or re-presentation to the emergency department occurred after discharge, compared to 4.9% before the use of clinical pathways. No adverse events were reported in these children. In 76 cases deviation from a clinical pathway process was reported. High parental satisfaction was reported for clinical pathways throughout the study. Clinical pathways in this emergency department allowed rapid stabilisation of children, reducing admission rate, with a shortened length of hospital stay and few patients re-presenting after discharge and were well accepted by parents.

Asthma↗
PubMed2006

Role of CXC chemokine receptor 3 pathway in renal ischemic injury.

Chemokines play a major role in the recruitment of leukocytes in inflammation and in the regulation of T helper 1 (Th1)/Th2 immune responses. These mechanisms have been recognized to be important in the pathogenesis of renal ischemia-reperfusion (I/R) injury. The interaction of the CXC chemokine receptor 3 (CXCR3) receptor with its ligands is a key pathogenic pathway in promoting inflammation and in enhancing Th1 immune responses. After the induction of ischemia in the mouse model of renal ischemia, an increase in intrarenal expression of CXCR3 and its ligands was observed. Compared with the wild-type (WT) mice, CXCR3-deficient mice (CXCR3-/-) had significantly lower serum creatinine levels, better survival rate, and significantly less acute tubular necrosis and cellular infiltrates. In the kidney, intracellular staining of infiltrating cells that were recovered from kidneys revealed a lower percentage of CD4+IFN-gamma+ cells in the CXCR3-/- mice compared with the WT mice. Furthermore, adoptive transfer of WT CD3+ cells into CXCR3-/- mice before induction of I/R injury abrogated the protection of CXCR3-/- mice from I/R injury. It is concluded that CXCR3 plays an important role in orchestrating the recruitment of Th1 cells to the ischemic kidney and in mediating I/R injury and therefore may serve as a novel target for the therapy of I/R injury.

Analysis of Variance↗
PubMed1997

Fear conditioning induces a lasting potentiation of synaptic currents in vitro.

The amygdala plays a critical role in the mediation of emotional responses, particularly fear, in both humans and animals. Fear conditioning, a conditioned learning paradigm, has served as a model for emotional learning in animals, and the neuroanatomical circuitry underlying the auditory fear-conditioning paradigm is well characterized. Synaptic transmission in the medial geniculate nucleus (MGN) to lateral nucleus of the amygdala (LA) pathway, a key segment of the auditory fear conditioning circuit, is mediated largely through N-methyl-D-aspartate (NMDA) and non-NMDA (such as alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)) glutamate receptors; the potential for neural plasticity in this pathway is suggested by its capacity to support long-term potentiation (LTP). Here we report a long-lasting increase in the synaptic efficacy of the MGN-LA pathway attributable to fear-conditioning itself, rather than an electrically induced model of learning. Fear-conditioned animals show a presynaptic facilitation of AMPA-receptor-mediated transmission, directly measured in vitro with whole-cell recordings in lateral amygdala neurons. These findings represent one of the first in vitro measures of synaptic plasticity resulting from emotional learning by whole animals.

Amygdala↗
PubMed2001

Association of mitogen-activated protein kinase pathways with gingival epithelial cell responses to Porphyromonas gingivalis infection.

Mitogen-activated protein (MAP) kinase pathways are key factors in host signaling events and can also play important roles in the internalization of pathogenic bacteria by host cells. Porphyromonas gingivalis, a periodontal pathogen, can efficiently invade human gingival epithelial cells (GECs). In this study, we examined the activation of MAP kinase pathways in GECs infected with P. gingivalis. c-Jun N-terminal kinase (JNK) was activated after 5 min of infection with P. gingivalis, whereas noninvasive Streptococcus gordonii did not have a significant effect on JNK activation. In contrast, extracellular signal-regulated kinase (ERK) 1/2 was downregulated in a dose-dependent manner by P. gingivalis, but not by S. gordonii, after a 15-min exposure. Nonmetabolically active P. gingivalis cells were unable to modulate MAP kinase activity. U0126, a specific inhibitor of MEK1/2 (ERK1/2 kinase), and toxin B, a specific inhibitor of Rho family GTPases, had no effect on P. gingivalis invasion. Genistein, a tyrosine protein kinase inhibitor, blocked uptake of P. gingivalis. The transcriptional regulator NF-kappaB was not activated by P. gingivalis. These results suggest that P. gingivalis can selectively target components of the MAP kinase pathways. ERK1/2, while not involved in P. gingivalis invasion of GECs, may be downregulated by internalized P. gingivalis. Activation of JNK is associated with the invasive process of P. gingivalis.

Butadienes↗
PubMed1999

The complexity of radiation stress responses: analysis by informatics and functional genomics approaches.

Molecular responses to genotoxic stress are complex and are mediated by a variety of regulatory pathways. One key element in cellular response is the stress gene transcription factor p53, which can regulate nearly 100 genes that have already been identified. Although p53 plays a central role in the cellular response to DNA-damaging agents such as ionizing radiation (IR), other pathways can also have important roles. One example is the transcriptional responses associated with IR-induced apoptosis, where induction of some genes is limited to p53 wild-type (wt) cells that also have the ability to undergo rapid apoptosis after irradiation. In contrast, other genes are triggered after IR in lines undergoing rapid apoptosis regardless of p53 status. From this and other examples, it is apparent that the pattern of stress gene expression is cell type specific in both primary and transformed lines. The premise will be developed that such differences in stress gene responsiveness can be employed as molecular markers using a combination of informatics and functional genomics approaches. An example is given using the panel of lines of the NCI anticancer drug screen where both the p53 status and sensitivity to a large collection of cytotoxic agents have been determined. The utility of cDNA microarray hybridization to measure IR-stress gene responses has recently been demonstrated and a large number of additional IR-stress genes have been identified. The responses of some of these genes to IR and other DNA-damaging agents varied widely in cell lines from different tissues of origin and different genetic backgrounds, highlighting the importance of cellular context to genotoxic stress responses; this also highlights the need for informatics approaches to discover and prioritize hypotheses regarding the importance of particular cellular factors. The aim of this review is to demonstrate the utility of combining an informatics approach with functional genomics in the study of stress responses.

Animals↗
PubMed2024

Proteomic analysis illustrates the potential involvement of dysregulated ribosome-related pathways and disrupted metabolism during retinoic acid-induced cleft palate development.

Recent studies have unveiled disrupted metabolism in the progression of cleft palate (CP), a congenital anomaly characterized by defective fusion of facial structures. Nonetheless, the precise composition of this disrupted metabolism remains elusive, prompting us to identify these components and elucidate primary metabolic irregularities contributing to CP pathogenesis. We established a murine CP model by retinoic acid (RA) treatment and analyzed control and RA-treated embryonic palatal tissues by LC-MS-based proteomic approach. We identified 220 significantly upregulated and 224 significantly downregulated proteins. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis revealed that these differentially expressed proteins (DEPs) were involved in translation, ribosome assembly, mitochondrial function, mRNA binding, as well as key metabolic pathways like oxidative phosphorylation (OXPHOS), glycolysis/gluconeogenesis, and amino acid biosynthesis. These findings suggest that dysregulated ribosome-related pathways and disrupted metabolism play a critical role in CP development. Protein-protein interaction analysis using the STRING database revealed a tightly connected network of DEPs. Furthermore, we identified the top 10 hub proteins in CP using the Cytohubba plugin in Cytoscape. These hub proteins, including RPL8, RPS11, ALB, PA2G4, RPL23, RPS6, CCT7, EGFR, HSPD1, and RPS28, are potentially key regulators of CP pathogenesis. In conclusion, our comprehensive proteomic analysis provides insights into the molecular alterations associated with RA-induced CP in Kun Ming mice. These findings suggest potential therapeutic targets and pathways to understand and prevent congenital craniofacial anomalies.

Cleft Palate↗
PubMed2004

The Arabidopsis thaliana chloroplast proteome reveals pathway abundance and novel protein functions.

BACKGROUND: Chloroplasts are plant cell organelles of cyanobacterial origin. They perform essential metabolic and biosynthetic functions of global significance, including photosynthesis and amino acid biosynthesis. Most of the proteins that constitute the functional chloroplast are encoded in the nuclear genome and imported into the chloroplast after translation in the cytosol. Since protein targeting is difficult to predict, many nuclear-encoded plastid proteins are still to be discovered. RESULTS: By tandem mass spectrometry, we identified 690 different proteins from purified Arabidopsis chloroplasts. Most proteins could be assigned to known protein complexes and metabolic pathways, but more than 30% of the proteins have unknown functions, and many are not predicted to localize to the chloroplast. Novel structure and function prediction methods provided more informative annotations for proteins of unknown functions. While near-complete protein coverage was accomplished for key chloroplast pathways such as carbon fixation and photosynthesis, fewer proteins were identified from pathways that are downregulated in the light. Parallel RNA profiling revealed a pathway-dependent correlation between transcript and relative protein abundance, suggesting gene regulation at different levels. CONCLUSIONS: The chloroplast proteome contains many proteins that are of unknown function and not predicted to localize to the chloroplast. Expression of nuclear-encoded chloroplast genes is regulated at multiple levels in a pathway-dependent context. The combined shotgun proteomics and RNA profiling approach is of high potential value to predict metabolic pathway prevalence and to define regulatory levels of gene expression on a pathway scale.

Arabidopsis↗
PubMed2006

No double-dissociation between optic ataxia and visual agnosia: multiple sub-streams for multiple visuo-manual integrations.

The current dominant view of the visual system is marked by the functional and anatomical dissociation between a ventral stream specialised for perception and a dorsal stream specialised for action. The "double-dissociation" between visual agnosia (VA), a deficit of visual recognition, and optic ataxia (OA), a deficit of visuo-manual guidance, considered as consecutive to ventral and dorsal damage, respectively, has provided the main argument for this dichotomic view. In the first part of this paper, we show that the currently available empirical data do not suffice to support a double-dissociation between OA and VA. In the second part, we review evidence coming from human neuropsychology and monkey data, which cast further doubts on the validity of a simple double-dissociation between perception and action because they argue for a far more complex organisation with multiple parallel visual-to-motor connections: 1. A dorso-dorsal pathway (involving the most dorsal part of the parietal and pre-motor cortices): for immediate visuo-motor control--with OA as typical disturbance. The latest research about OA is reviewed, showing how these patients exhibit deficits restricted to the most direct and fast visuo-motor transformations. We also propose that mild mirror ataxia, consisting of misreaching errors when the controlesional hand is guided to a visual goal though a mirror, could correspond to OA with an isolated "hand effect". 2. A ventral stream-prefrontal pathway (connections from the ventral visual stream to pre-frontal areas, by-passing the parietal areas): for "mediate" control (involving spatial or temporal transpositions [Rossetti, Y., & Pisella, L. (2003). Mediate responses as direct evidence for intention: Neuropsychology of Not to-, Not now- and Not there-tasks. In S. Johnson (Ed.), Cognitive Neuroscience perspectives on the problem of intentional action (pp. 67-105). MIT Press.])--with VA as typical disturbance. Preserved visuo-manual guidance in patients with VA is restricted to immediate goal-directed guidance, they exhibit deficits for delayed or pantomimed actions. 3. A ventro-dorsal pathway (involving the more ventral part of the parietal lobe and the pre-motor and pre-frontal areas): for complex planning and programming relying on high representational levels with a more bilateral organisation or an hemispheric lateralisation--with mirror apraxia, limb apraxia and spatial neglect as representatives. Mirror apraxia is a deficit that affects both hands after unilateral inferior parietal lesion with the patients reaching systematically and repeatedly toward the virtual image in the mirror. Limb apraxia is localized on a more advanced conceptual level of object-related actions and results from deficient integrative, computational and "working memory" capacities of the left inferior parietal lobule. A component of spatial working memory has recently been revealed also in spatial neglect consecutive to lesion involving the network of the right inferior parietal lobule and the right frontal areas. We conclude by pointing to the differential temporal constraints and integrative capabilities of these parallel visuo-motor pathways as keys to interpret the neuropsychological deficits.

Agnosia↗
PubMedDate not supplied

Molecular mechanisms and pathways in bladder cancer development and progression.

BACKGROUND: The basis for bladder cancer development and progression is complex and involves genetic abnormalities. These abnormalities yield phenotypic changes that allow normal transitional cells to become cancerous and finally acquire the "malignant phenotype." METHODS: The authors review the most common genetic alterations in bladder cancer and the molecular mechanisms and pathways involved in the conversion of normal transitional cell into malignant transitional cancer cells. RESULTS: There are several potential genetic changes of the urothelium that eventually cause bladder cancer initiation and tumor progression. Some of these alterations are also found in other malignancies suggesting that key common pathways exist in the development of cancer. CONCLUSIONS: As the roles of certain genes or proteins are further elucidated, a better understanding of cancer development can aid in the prevention, diagnosis, and treatment of bladder cancer.

Carcinoma, Transitional Cell↗
PubMed2001

Activating Ly-49 NK receptors: central role in cytokine and chemokine production.

In an attempt to understand potential novel functions of receptors in vivo, we evaluated gene expression after cross-linking the activating Ly-49D mouse NK receptor. Gene expression was evaluated using a mouse GEM 2 microarray chip (Incyte Genomics, St. Louis, MO). Each chip displays a total of 8734 elements. The strongly induced genes fell into two categories: 1) soluble factors and 2) apoptotic genes. The majority of the strongly induced mRNAs as analyzed by microarray hybridization were chemokine genes. RNase protection assays and chemokine protein production analysis validated the microarray results, as cross-linking the Ly-49D mouse NK receptor induced high levels of IFN-gamma, lymphotactin, macrophage-inflammatory protein (MIP)1alpha, and MIP1beta. This gene expression was specific because other chemokines were not induced by anti-Ly-49D receptors. In addition, a series of pharmacological inhibitors were used to identify the key signaling pathways involved in the cellular response. The primary Ly-49D signaling for IFN-gamma production is predominantly mediated through Src kinase pathways involving membrane proximal events, whereas MIP1alpha and MIP1beta gene induction is more complex and may involve multiple biochemical pathways. Thus, we conclude that a primary role for the activating NK receptors in vivo may be to trigger soluble factor production and regulation of the immune response. This would place NK cells and their activating Ly-49 receptors as important initiators of microbial immunity and key elements of the innate immune system.

Animals↗
PubMed2004

Blockade of receptor for advanced glycation end product (RAGE) attenuates ischemia and reperfusion injury to the liver in mice.

Hepatic ischemia/reperfusion (I/R) injury associated with liver transplantation and hepatic resection is characterized by hepatocellular damage and a deleterious inflammatory response. In this study, we examined whether receptor for advanced glycation end product (RAGE) activation is linked to mechanisms accentuating inflammation on I/R in a murine model of total hepatic ischemia. Animals treated with soluble RAGE (sRAGE), the extracellular ligand-binding domain of RAGE, displayed increased survival after total hepatic I/R compared with vehicle treatment. TUNEL assay and histologic analysis revealed that blockade of RAGE was highly protective against hepatocellular death and necrosis on I/R; in parallel, proliferating cell nuclear antigen was enhanced in livers of mice treated with sRAGE. Rapid activation of p38, p44/42, stress-activated protein kinase and c-Jun N-terminal kinase mitogen-activated protein kinases, signal transducer and activator of transcription-3, and nuclear translocation of activator protein-1 was evident at early times on I/R. In the remnants of sRAGE-treated livers, however, activation of each of these signaling and transcription factor pathways was strikingly decreased. sRAGE-treated remnants displayed enhanced activation of nuclear factor kappaB, in parallel with increased transcripts for the proregenerative cytokine, tumor necrosis factor-alpha. In conclusion, these data suggest that RAGE modulates hepatic I/R injury, at least in part by activation of key signaling pathways linked to proinflammatory and cell death-promoting responses. We propose that blockade of this pathway may represent a novel strategy to attenuate injury in hepatic I/R and to facilitate regeneration.

Animals↗
PubMed2004

Microbial colonization and atopic dermatitis.

PURPOSE OF REVIEW: Atopic dermatitis is a chronic relapsing, pruritic inflammation of the skin, affecting 10-20% of children and 1-3% adults worldwide, with increasing prevalence in highly industrialized countries. Here we review relevant studies, published since June 2002, about immunological triggers in atopic dermatitis, with emphasis on the role of microbial colonization. RECENT FINDINGS: During the past 2 years there has been considerable interest in the mechanisms and trigger factors underlying the increased microbial colonization of atopic skin. Staphylococcus aureus appears to play a significant role as it leads to a worsening of disease severity by producing superantigens that induce a strong proliferation of T cells and favour a T helper type 2-like cytokine profile. In addition, different Malassezia species seem to elicit and maintain skin inflammation after sensitization, but the precise immunological pathway has not yet been described. All these microorganisms are not only perceived as aetiological factors but also as agents responsible either for sustained disease activity or resistance to therapy by modulation of the immune response. SUMMARY: New insights into the important role of microorganisms and their key immunomodulatory pathways in atopic dermatitis may have important implications from a therapeutic point of view because patients with atopic dermatitis may benefit from more than just anti-inflammatory treatment in the future.

Adolescent↗
PubMed2025

Pathway-specific genomic alterations in pancreatic cancer across diverse cohorts.

BACKGROUND/OBJECTIVES: Pancreatic cancer (PC) is an aggressive malignancy with rising incidence and poor survival rates. While Hispanic/Latino (H/L) patients have a lower overall incidence compared to Non-Hispanic White (NHW) patients, they are diagnosed at younger ages, often present with more advanced disease, and experience worse survival outcomes. The molecular drivers underlying these disparities remain poorly understood. Key oncogenic pathways, including TP53, WNT, PI3K, TGF-Beta, and RTK/RAS, play crucial roles in tumor progression, therapy resistance, and response to targeted treatments. However, their ethnicity-specific alterations and prognostic implications in PC remain largely unexplored. This study aims to characterize pathway-specific mutations in PC among H/L and NHW patients, assess tumor mutation burden, and identify ethnicity-specific oncogenic drivers using publicly available datasets. The findings may provide critical insights to optimize precision medicine strategies and enhance targeted therapies for underrepresented populations. METHODS: A bioinformatics analysis was performed using publicly available PC datasets to evaluate mutation frequencies in genes associated with the TGF-Beta, RTK/RAS, WNT, PI3K, and TP53 pathways. The study included 4,248 patients, with 407 identified as H/L and 3,841 as NHW. Patients were stratified by ethnicity to assess differences in mutation prevalence. Chi-squared tests were conducted to compare mutation rates between groups, while Kaplan-Meier survival analysis was performed to evaluate overall survival differences based on pathway-specific alterations. RESULTS: Significant differences were observed in the TGF-Beta pathway between H/L and NHW patients. TGF-Beta mutations were less prevalent in H/L patients (18.4% vs. 24.4%, p = 8.6e-3). Additionally, genes related to the TGF-Beta pathway showed significant alterations, with SMAD2 (1.5% vs. 0.4%, p = 6.3e-3) and SMAD4 (15% vs. 19.9%, p = 0.02) exhibiting notable differences. Although RTK/RAS, WNT, PI3K, and TP53 pathway mutations were not statistically significant overall, borderline significance was observed in genes associated with these pathways, including ERBB4 (3.4% vs. 1.8%, p = 0.03), ALK (2.7% vs. 1.1%, p = 0.01), HRAS (1.2% vs. 0.1%, p = 1.3e-4), and RIT1 (0.7% vs. 0.1%, p = 0.03) in the RTK/RAS pathway, as well as CTNNB1 (2.9% vs. 1.3%, p = 0.01) in the WNT pathway. Survival analysis revealed no significant differences in overall survival among H/L patients. However, NHW patients with TP53 pathway alterations exhibited borderline significant differences in survival outcomes.

PI3K pathway↗
PubMed2000

Chlorophyll breakdown in oilseed rape.

Chlorophyll catabolism accompanying leaf senescence is one of the most spectacular natural phenomena. Despite this fact, the metabolism of chlorophyll has been largely neglegted until recently. Oilseed rape has been used extensively as a model plant for the recent elucidating of structures of chlorophyll catabolites and for investigation of the enzymic reactions of the chlorophyll breakdown pathway. The key reaction which causes loss of green color is catalyzed in a two-step reaction by pheophorbide a oxygenase and red chlorophyll catabolite reductase. In this Minireview, we summarize the actual knowledge about catabolites and enzymes of chlorophyll catabolism in oilseed rape and discuss the significance of this pathway in respect to chlorophyll degradation during Brassica napus seed development.

Journal Article↗