Arabidopsis inositol phosphate kinases, IPK1 and ITPK1, constitute a metabolic pathway in maintaining phosphate homeostasis

Emerging studies have implicated a close link between inositol phosphate (InsP) metabolism and cellular phosphate (Pi) homeostasis in eukaryotes; however, whether a common InsP species is deployed as an evolutionarily conserved metabolic messenger to mediate Pi signaling remains unknown. Here, using genetics and InsP profiling combined with Pi starvation response (PSR) analysis in Arabidopsis thaliana, we showed that the kinase activity of inositol pentakisphosphate 2‐kinase (IPK1), an enzyme required for phytate (inositol hexakisphosphates; InsP6) synthesis, is indispensable for maintaining Pi homeostasis under Pi‐replete conditions, and inositol 1,3,4‐trisphosphate 5/6‐kinase 1 (ITPK1) plays an equivalent role. Although both ipk1‐1 and itpk1 mutants exhibited decreased levels of InsP6 and diphosphoinositol pentakisphosphate (PP‐InsP5; InsP7), disruption of another ITPK family enzyme, ITPK4, which correspondingly caused depletion of InsP6 and InsP7, did not display similar Pi‐related phenotypes, which precludes these InsP species as effectors. Notably, the level of D/L‐Ins(3,4,5,6)P4 was concurrently elevated in both ipk1‐1 and itpk1 mutants, which showed a specific correlation to the misregulated Pi phenotypes. However, the level of D/L‐Ins(3,4,5,6)P4 is not responsive to Pi starvation that instead manifests a shoot‐specific increase in InsP7 level. This study demonstrates a more nuanced picture of the intersection of InsP metabolism and Pi homeostasis and PSR than has previously been elaborated and additionally establishes intermediate steps to phytate biosynthesis in plant vegetative tissues

The Agricultural Matrix and a Future Paradigm for Conservation

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/73889/1/j.1523-1739.2006.00582.x.pd

Life-Long Implications of Developmental Exposure to Environmental Stressors: New Perspectives

The Developmental Origins of Health and Disease (DOHaD) paradigm is one of the most rapidly expanding areas of biomedical research. Environmental stressors that can impact on DOHaD encompass a variety of environmental and occupational hazards as well as deficiency and oversupply of nutrients and energy. They can disrupt early developmental processes and lead to increased susceptibility to disease/dysfunctions later in life. Presentations at the fourth Conference on Prenatal Programming and Toxicity in Boston, in October 2014, provided important insights and led to new recommendations for research and public health action. The conference highlighted vulnerable exposure windows that can occur as early as the preconception period and epigenetics as a major mechanism than can lead to disadvantageous "reprogramming" of the genome, thereby potentially resulting in transgenerational effects. Stem cells can also be targets of environmental stressors, thus paving another way for effects that may last a lifetime. Current testing paradigms do not allow proper characterization of risk factors and their interactions. Thus, relevant exposure levels and combinations for testing must be identified from human exposure situations and outcome assessments. Testing of potential underpinning mechanisms and biomarker development require laboratory animal models and in vitro approaches. Only few large-scale birth cohorts exist, and collaboration between birth cohorts on a global scale should be facilitated. DOHaD-based research has a crucial role in establishing factors leading to detrimental outcomes and developing early preventative/remediation strategies to combat these risks.status: publishe

Life-Long Implications of Developmental Exposure to Environmental Stressors: New Perspectives

The Developmental Origins of Health and Disease (DOHaD) paradigm is one of the most rapidly expanding areas of biomedical research. Environmental stressors that can impact on DOHaD encompass a variety of environmental and occupational hazards as well as deficiency and oversupply of nutrients and energy. They can disrupt early developmental processes and lead to increased susceptibility to disease/dysfunctions later in life. Presentations at the fourth Conference on Prenatal Programming and Toxicity in Boston, in October 2014, provided important insights and led to new recommendations for research and public health action. The conference highlighted vulnerable exposure windows that can occur as early as the preconception period and epigenetics as a major mechanism than can lead to disadvantageous “reprogramming” of the genome, thereby potentially resulting in transgenerational effects. Stem cells can also be targets of environmental stressors, thus paving another way for effects that may last a lifetime. Current testing paradigms do not allow proper characterization of risk factors and their interactions. Thus, relevant exposure levels and combinations for testing must be identified from human exposure situations and outcome assessments. Testing of potential underpinning mechanisms and biomarker development require laboratory animal models and in vitro approaches. Only few large-scale birth cohorts exist, and collaboration between birth cohorts on a global scale should be facilitated. DOHaD-based research has a crucial role in establishing factors leading to detrimental outcomes and developing early preventative/remediation strategies to combat these risks. The Developmental Origins of Health and Disease (DOHaD) paradigm is one of the most rapidly expanding areas of biomedical research today. This field originated with early observations that malnutrition and low-level exposures to drugs and toxic substances (eg, alcohol and methylmercury) might be well tolerated by a pregnant woman, but her gestating fetus would be afflicted by adverse effects, some of which might become apparent only later in life (1, 2). The field has now broadened to encompass consideration of a variety of environmental and occupational hazards, whether chemical, physical, or biological, and both deficiency and oversupply of nutrients and energy. When these environmental stressors disrupt early developmental processes they may cause changes in cellular gene expression, cell numbers or location of cells that persist and then lead to increased susceptibility to disease/dysfunctions later in life. The fourth Conference on Prenatal Programming and Toxicity (PPTOX IV) in Boston, October, 2014, brought together researchers interested in understanding the role of environmental stressors in developmental programming. As before (3, 4), the goal of the conference was to stimulate and exchange research results and to discuss their implications and how to further develop and strengthen research in this field. This article presents a brief summary of important insights and recommendations that emerged from the conference presentations and discussion sessions. Figure 1 outlines the major issues discussed. Abstracts and presentations are available at the conference web site (http://www.endocrine.org/meetings/pptox-iv). - See more at: http://press.endocrine.org/doi/10.1210/EN.2015-1350#sthash.ocQ8rPcQ.dpu

Life-long implications of developmental exposure to environmental stressors: New perspectives

The Developmental Origins of Health and Disease (DOHaD) paradigm is one of the most rapidly expanding areas of biomedical research. Environmental stressors that can impact on DOHaD encompass a variety of environmental and occupational hazards as well as deficiency and oversupply of nutrients and energy. They can disrupt early developmental processes and lead to increased susceptibility to disease/dysfunctions later in life. Presentations at the fourth Conference on Prenatal Programming and Toxicity in Boston, in October 2014, provided important insights and led to new recommendations for research and public health action. The conference highlighted vulnerable exposure windows that can occur as early as the preconception period and epigenetics as a major mechanism than can lead to disadvantageous “reprogramming” of the genome, thereby potentially resulting in transgenerational effects. Stem cells can also be targets of environmental stressors, thus paving another way for effects that may last a lifetime. Current testing paradigms do not allow proper characterization of risk factors and their interactions. Thus, relevant exposure levels and combinations for testing must be identified from human exposure situations and outcome assessments. Testing of potential underpinning mechanisms and biomarker development require laboratory animal models and in vitro approaches. Only few large-scale birth cohorts exist, and collaboration between birth cohorts on a global scale should be facilitated. DOHaD-based research has a crucial role in establishing factors leading to detrimental outcomes and developing early preventative/remediation strategies to combat these risks