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  1. Article ; Online: A nucleotide diphosphate kinase mediates tethering between mitochondria prior to fusion.

    Ikeda, Arisa / Iijima, Miho / Sesaki, Hiromi

    The Journal of cell biology

    2023  Volume 222, Issue 10

    Abstract: Mitochondrial fusion plays an important role in both their structure and function. In this issue, Su et al. (2023. J. Cell Biol.https://doi.org/10.1083/jcb.202301091) report that a nucleoside diphosphate kinase, NME3, facilitates mitochondrial tethering ... ...

    Abstract Mitochondrial fusion plays an important role in both their structure and function. In this issue, Su et al. (2023. J. Cell Biol.https://doi.org/10.1083/jcb.202301091) report that a nucleoside diphosphate kinase, NME3, facilitates mitochondrial tethering prior to fusion through its direct membrane-binding and hexamerization but not its kinase activity.
    MeSH term(s) Diphosphates ; Mitochondria/genetics ; Mitochondrial Dynamics ; Nucleotides ; Phosphorylation ; Humans ; NM23 Nucleoside Diphosphate Kinases/genetics
    Chemical Substances Diphosphates ; Nucleotides ; NME3 protein, human (EC 2.7.4.6) ; NM23 Nucleoside Diphosphate Kinases
    Language English
    Publishing date 2023-09-14
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 218154-x
    ISSN 1540-8140 ; 0021-9525
    ISSN (online) 1540-8140
    ISSN 0021-9525
    DOI 10.1083/jcb.202309037
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  2. Article ; Online: Role of human HSPE1 for OPA1 processing independent of HSPD1.

    Yeung, Nelson / Murata, Daisuke / Iijima, Miho / Sesaki, Hiromi

    iScience

    2023  Volume 26, Issue 2, Page(s) 106067

    Abstract: The human mtHSP60/HSPD1-mtHSP10/HSPE1 system prevents protein misfolding and maintains proteostasis in the mitochondrial matrix. Altered activities of this chaperonin system have been implicated in human diseases, such as cancer and neurodegeneration. ... ...

    Abstract The human mtHSP60/HSPD1-mtHSP10/HSPE1 system prevents protein misfolding and maintains proteostasis in the mitochondrial matrix. Altered activities of this chaperonin system have been implicated in human diseases, such as cancer and neurodegeneration. However, how defects in HSPD1 and HSPE1 affect mitochondrial structure and dynamics remains elusive. In the current study, we address this fundamental question in a human cell line, HEK293T. We found that the depletion of HSPD1 or HSPE1 results in fragmentation of mitochondria, suggesting a decrease in mitochondrial fusion. Supporting this notion, HSPE1 depletion led to proteolytic inactivation of OPA1, a dynamin-related GTPase that fuses the mitochondrial membrane. This OPA1 inactivation was mediated by a stress-activated metalloprotease, OMA1. In contrast, HSPD1 depletion did not induce OMA1 activation or OPA1 cleavage. These data suggest that HSPE1 controls mitochondrial morphology through a mechanism separate from its chaperonin activity.
    Language English
    Publishing date 2023-01-26
    Publishing country United States
    Document type Journal Article
    ISSN 2589-0042
    ISSN (online) 2589-0042
    DOI 10.1016/j.isci.2023.106067
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  3. Article ; Online: Role of human HSPE1 for OPA1 processing independent of HSPD1

    Nelson Yeung / Daisuke Murata / Miho Iijima / Hiromi Sesaki

    iScience, Vol 26, Iss 2, Pp 106067- (2023)

    2023  

    Abstract: Summary: The human mtHSP60/HSPD1-mtHSP10/HSPE1 system prevents protein misfolding and maintains proteostasis in the mitochondrial matrix. Altered activities of this chaperonin system have been implicated in human diseases, such as cancer and ... ...

    Abstract Summary: The human mtHSP60/HSPD1-mtHSP10/HSPE1 system prevents protein misfolding and maintains proteostasis in the mitochondrial matrix. Altered activities of this chaperonin system have been implicated in human diseases, such as cancer and neurodegeneration. However, how defects in HSPD1 and HSPE1 affect mitochondrial structure and dynamics remains elusive. In the current study, we address this fundamental question in a human cell line, HEK293T. We found that the depletion of HSPD1 or HSPE1 results in fragmentation of mitochondria, suggesting a decrease in mitochondrial fusion. Supporting this notion, HSPE1 depletion led to proteolytic inactivation of OPA1, a dynamin-related GTPase that fuses the mitochondrial membrane. This OPA1 inactivation was mediated by a stress-activated metalloprotease, OMA1. In contrast, HSPD1 depletion did not induce OMA1 activation or OPA1 cleavage. These data suggest that HSPE1 controls mitochondrial morphology through a mechanism separate from its chaperonin activity.
    Keywords Biological sciences ; Molecular biology ; Cell biology ; Science ; Q
    Subject code 570
    Language English
    Publishing date 2023-02-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
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  4. Article ; Online: An AAA-ATPase links mitochondrial division with DNA nucleoids.

    Yeung, Nelson / Iijima, Miho / Sesaki, Hiromi

    Proceedings of the National Academy of Sciences of the United States of America

    2022  Volume 119, Issue 51, Page(s) e2217949119

    MeSH term(s) ATPases Associated with Diverse Cellular Activities ; Mitochondrial Dynamics ; DNA, Mitochondrial/genetics ; Mitochondrial Proteins/metabolism
    Chemical Substances ATPases Associated with Diverse Cellular Activities (EC 3.6.4.-) ; DNA, Mitochondrial ; Mitochondrial Proteins
    Language English
    Publishing date 2022-12-12
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Comment
    ZDB-ID 209104-5
    ISSN 1091-6490 ; 0027-8424
    ISSN (online) 1091-6490
    ISSN 0027-8424
    DOI 10.1073/pnas.2217949119
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  5. Article ; Online: Protocol for measuring mitochondrial size in mouse and human liver tissues.

    Ramatchandirin, Balamurugan / Iijima, Miho / Ikeda, Arisa / Pearah, Alexia / Radovick, Sally / Wondisford, Fredric E / Sesaki, Hiromi / He, Ling

    STAR protocols

    2024  Volume 5, Issue 1, Page(s) 102842

    Abstract: Mitochondrial dynamic process is important for cell viability, metabolic activity, and mitochondria health. Here, we present a protocol for measuring mitochondrial size through immunofluorescence staining, confocal imaging, and analysis in ImageJ. We ... ...

    Abstract Mitochondrial dynamic process is important for cell viability, metabolic activity, and mitochondria health. Here, we present a protocol for measuring mitochondrial size through immunofluorescence staining, confocal imaging, and analysis in ImageJ. We describe the steps for tissue processing, antigen retrieval, mitochondrial staining using an integrating immunofluorescence assay, and computerized image analysis to measure each mitochondrial size in mouse and human liver tissues. This protocol reduces tissue sample volume and processing time for the preparation of primary cells. For complete details on the use and execution of this protocol, please refer to Pearah et al.
    MeSH term(s) Humans ; Animals ; Mice ; Mitochondrial Size ; Liver ; Cell Survival ; Image Processing, Computer-Assisted ; Mitochondria
    Language English
    Publishing date 2024-01-18
    Publishing country United States
    Document type Journal Article
    ISSN 2666-1667
    ISSN (online) 2666-1667
    DOI 10.1016/j.xpro.2024.102842
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  6. Article ; Online: Protocol for measuring mitochondrial size in mouse and human liver tissues

    Balamurugan Ramatchandirin / Miho Iijima / Arisa Ikeda / Alexia Pearah / Sally Radovick / Fredric E. Wondisford / Hiromi Sesaki / Ling He

    STAR Protocols, Vol 5, Iss 1, Pp 102842- (2024)

    2024  

    Abstract: Summary: Mitochondrial dynamic process is important for cell viability, metabolic activity, and mitochondria health. Here, we present a protocol for measuring mitochondrial size through immunofluorescence staining, confocal imaging, and analysis in ... ...

    Abstract Summary: Mitochondrial dynamic process is important for cell viability, metabolic activity, and mitochondria health. Here, we present a protocol for measuring mitochondrial size through immunofluorescence staining, confocal imaging, and analysis in ImageJ. We describe the steps for tissue processing, antigen retrieval, mitochondrial staining using an integrating immunofluorescence assay, and computerized image analysis to measure each mitochondrial size in mouse and human liver tissues. This protocol reduces tissue sample volume and processing time for the preparation of primary cells.For complete details on the use and execution of this protocol, please refer to Pearah et al.1 : Publisher’s note: Undertaking any experimental protocol requires adherence to local institutional guidelines for laboratory safety and ethics.
    Keywords Cell Biology ; Health Sciences ; Metabolism ; Science (General) ; Q1-390
    Language English
    Publishing date 2024-03-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
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  7. Article ; Online: Generating a new mouse model for nuclear PTEN deficiency by a single K13R mutation.

    Kato, Takashi / Igarashi, Atsushi / Sesaki, Hiromi / Iijima, Miho

    Genes to cells : devoted to molecular & cellular mechanisms

    2021  Volume 26, Issue 12, Page(s) 1014–1022

    Abstract: Many human diseases, including cancer and neurological abnormalities, are linked to deficiencies of phosphatase and tensin homolog deleted on chromosome ten (PTEN), a dual phosphatase that dephosphorylates both lipids and proteins. PTEN functions in ... ...

    Abstract Many human diseases, including cancer and neurological abnormalities, are linked to deficiencies of phosphatase and tensin homolog deleted on chromosome ten (PTEN), a dual phosphatase that dephosphorylates both lipids and proteins. PTEN functions in multiple intracellular locations, including the plasma membrane and nucleus. Therefore, a critical challenge to understand the pathogenesis of PTEN-associated diseases is to determine the specific role of PTEN at different locations. Toward this goal, the current study generated a mouse line in which lysine 13, which is critical for the nuclear localization of PTEN, is changed to arginine in the lipid-binding domain using the CRISPR-Ca9 gene-editing system. We found that PTEN
    MeSH term(s) Animals ; Cell Nucleus/metabolism ; Disease Models, Animal ; Mice ; Mutation ; Neurons/metabolism ; PTEN Phosphohydrolase/genetics ; PTEN Phosphohydrolase/metabolism ; Phosphorylation
    Chemical Substances PTEN Phosphohydrolase (EC 3.1.3.67)
    Language English
    Publishing date 2021-10-28
    Publishing country England
    Document type Journal Article
    ZDB-ID 1330000-3
    ISSN 1365-2443 ; 1356-9597
    ISSN (online) 1365-2443
    ISSN 1356-9597
    DOI 10.1111/gtc.12902
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    Zs.A 4539: Show issues Location:
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  8. Article ; Online: Nuclear PTEN deficiency and heterozygous PTEN loss have distinct impacts on brain and lymph node size.

    Igarashi, Atsushi / Kato, Takashi / Sesaki, Hiromi / Iijima, Miho

    Biochemical and biophysical research communications

    2021  Volume 555, Page(s) 81–88

    Abstract: Defects in PTEN, a critical tumor suppressor, are associated with tumorigenesis and aberrant organ sizes. It has been shown that heterozygous PTEN loss increases brains and neuron size, while the specific loss of nuclear PTEN has the opposite effect. ... ...

    Abstract Defects in PTEN, a critical tumor suppressor, are associated with tumorigenesis and aberrant organ sizes. It has been shown that heterozygous PTEN loss increases brains and neuron size, while the specific loss of nuclear PTEN has the opposite effect. Here, we investigate the impact of a combination of heterozygous PTEN loss and nuclear PTEN loss on the size of various organs, including the brain, liver, thymus, spleen, and inguinal lymph node. We found that the effect of the combination varies among organs. Notably, the combination of heterozygous PTEN loss and nuclear PTEN loss restored the normal size of brains and neurons. In contrast, the liver's size was unaffected by either single PTEN defects or their combination. Strikingly, the size of the inguinal lymph node was greatly increased due to lymphoma by the combination of the two PTEN defects. These data suggest that nuclear PTEN and non-nuclear PTEN function in an antagonistic manner in the brain while acting synergistically in the inguinal lymph node.
    MeSH term(s) Animals ; Brain/anatomy & histology ; Brain/pathology ; Cell Nucleus/genetics ; Cell Nucleus/metabolism ; Heterozygote ; Lymph Nodes/pathology ; Mice, Knockout ; Mice, Transgenic ; Neurons/metabolism ; Neurons/pathology ; PTEN Phosphohydrolase/genetics ; PTEN Phosphohydrolase/metabolism ; Mice
    Chemical Substances PTEN Phosphohydrolase (EC 3.1.3.67) ; Pten protein, mouse (EC 3.1.3.67)
    Language English
    Publishing date 2021-04-01
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 205723-2
    ISSN 1090-2104 ; 0006-291X ; 0006-291X
    ISSN (online) 1090-2104 ; 0006-291X
    ISSN 0006-291X
    DOI 10.1016/j.bbrc.2021.03.081
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    Zs.A 116: Show issues Location:
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  9. Article ; Online: Long noncoding RNA TUG1 promotes cisplatin resistance in ovarian cancer via upregulation of DNA polymerase eta.

    Sonobe, Ryosuke / Yang, Peng / Suzuki, Miho M / Shinjo, Keiko / Iijima, Kenta / Nishiyama, Nobuhiro / Miyata, Kanjiro / Kataoka, Kazunori / Kajiyama, Hiroaki / Kondo, Yutaka

    Cancer science

    2024  

    Abstract: Chemoresistance is a major cause of high mortality and poor survival in patients with ovarian cancer (OVCA). Understanding the mechanisms of chemoresistance is urgently required to develop effective therapeutic approaches to OVCA. Here, we show that ... ...

    Abstract Chemoresistance is a major cause of high mortality and poor survival in patients with ovarian cancer (OVCA). Understanding the mechanisms of chemoresistance is urgently required to develop effective therapeutic approaches to OVCA. Here, we show that expression of the long noncoding RNA, taurine upregulated gene 1 (TUG1), is markedly upregulated in samples from OVCA patients who developed resistance to primary platinum-based therapy. Depletion of TUG1 increased sensitivity to cisplatin in the OVCA cell lines, SKOV3 and KURAMOCHI. Combination therapy of cisplatin with antisense oligonucleotides targeting TUG1 coupled with a drug delivery system effectively relieved the tumor burden in xenograft mouse models. Mechanistically, TUG1 acts as a competing endogenous RNA by downregulating miR-4687-3p and miR-6088, both of which target DNA polymerase eta (POLH), an enzyme required for translesion DNA synthesis. Overexpression of POLH reversed the effect of TUG1 depletion on cisplatin-induced cytotoxicity. Our data suggest that TUG1 upregulation allows OVCA to tolerate DNA damage via upregulation of POLH; this provides a strong rationale for targeting TUG1 to overcome cisplatin resistance in OVCA.
    Language English
    Publishing date 2024-04-01
    Publishing country England
    Document type Journal Article
    ZDB-ID 2115647-5
    ISSN 1349-7006 ; 1349-7006
    ISSN (online) 1349-7006
    ISSN 1349-7006
    DOI 10.1111/cas.16150
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  10. Article ; Online: Mitochondrial division, fusion and degradation.

    Murata, Daisuke / Arai, Kenta / Iijima, Miho / Sesaki, Hiromi

    Journal of biochemistry

    2019  Volume 167, Issue 3, Page(s) 233–241

    Abstract: The mitochondrion is an essential organelle for a wide range of cellular processes, including energy production, metabolism, signal transduction and cell death. To execute these functions, mitochondria regulate their size, number, morphology and ... ...

    Abstract The mitochondrion is an essential organelle for a wide range of cellular processes, including energy production, metabolism, signal transduction and cell death. To execute these functions, mitochondria regulate their size, number, morphology and distribution in cells via mitochondrial division and fusion. In addition, mitochondrial division and fusion control the autophagic degradation of dysfunctional mitochondria to maintain a healthy population. Defects in these dynamic membrane processes are linked to many human diseases that include metabolic syndrome, myopathy and neurodegenerative disorders. In the last several years, our fundamental understanding of mitochondrial fusion, division and degradation has been significantly advanced by high resolution structural analyses, protein-lipid biochemistry, super resolution microscopy and in vivo analyses using animal models. Here, we summarize and discuss this exciting recent progress in the mechanism and function of mitochondrial division and fusion.
    MeSH term(s) Actins/metabolism ; Animals ; Dynamins/genetics ; Dynamins/metabolism ; Endoplasmic Reticulum/metabolism ; GTP Phosphohydrolases/genetics ; GTP Phosphohydrolases/metabolism ; Humans ; Lipid Metabolism ; Mitochondria/enzymology ; Mitochondria/metabolism ; Mitochondrial Dynamics/genetics ; Mitophagy/genetics
    Chemical Substances Actins ; GTP Phosphohydrolases (EC 3.6.1.-) ; OPA1 protein, human (EC 3.6.1.-) ; Dynamins (EC 3.6.5.5)
    Language English
    Publishing date 2019-12-04
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 218073-x
    ISSN 1756-2651 ; 0021-924X
    ISSN (online) 1756-2651
    ISSN 0021-924X
    DOI 10.1093/jb/mvz106
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