Senescence,a crucial developmental process in the life cycle of plants,involves programmed destruction of cellular components of leaves.The onset of senescence is synchronized with other developmental processes for su...Senescence,a crucial developmental process in the life cycle of plants,involves programmed destruction of cellular components of leaves.The onset of senescence is synchronized with other developmental processes for successful reproduction since senescence eventually leads to cell death.Arabinosyltransferase FASCIATED AND BRANCHED 2(FAB2)is known to control meristem proliferation.Here,we show that FAB2 could inhibit premature leaf senescence in tomato plants.Both chemically mutagenized and CRISPR-generated fab2 mutants exhibited excessively accelerated senescence,which resulted in sterility.Transcriptome analysis revealed that FAB2 extended leaf longevity by suppressing transcription of genes highly expressed in mature leaves.Transcription of FAB2 was increased in younger leaves,potentially inhibiting premature leaf senescence.The precocious senescence of fab2 mutants was in contrast to fasciated inflorescence(fin)mutants,which carried mutations in a hydroxyproline O-arabinosyltransferase gene,leading to meristem overproliferation.Our observations indicate that complex genetic hierarchy in the cascade of tomato arabinosyltransferases could control different aspects of developmental processes such as stem cell proliferation and senescence.展开更多
Myelin-associated inhibitory factors within the central nervous system（CNS） are considered to be one of the main obstacles for axonal regeneration following disease or injury. The nogo receptor 1（NgR1） has been we...Myelin-associated inhibitory factors within the central nervous system（CNS） are considered to be one of the main obstacles for axonal regeneration following disease or injury. The nogo receptor 1（NgR1） has been well documented to play a key role in limiting axonal regrowth in the injured and diseased mammalian CNS. However, the role of nogo receptor in immune cell activation during CNS inflammation is yet to be mechanistically elucidated. Microglia/macrophages are immune cells that are regarded as pathogenic contributors to inflammatory demyelinating lesions in multiple sclerosis（MS）. In this study, the animal model of MS, experimental autoimmune encephalomyelitis（EAE） was induced in ngr1^＋/＋ and ngr1^–/– female mice following injection with the myelin oligodendrocyte glycoprotein（MOG_（35–55）） peptide. A fatemap analysis of microglia/macrophages was performed throughout spinal cord sections of EAE-induced mice at clinical scores of 0, 1, 2 and 3, respectively（increasing locomotor disability） from both genotypes, using the CD11 b and Iba1 cell markers. Western immunoblotting using lysates from isolated spinal cord microglia/macrophages, along with immunohistochemistry and flow cytometric analysis, was performed to demonstrate the expression of nogo receptor and its two homologs during EAE progression. Myelin protein engulfment during EAE progression in ngr1^＋/＋ and ngr1^–/– mice was demonstrated by western immunblotting of lysates from isolated spinal cord microglia/macrophages, detecting levels of Nogo-A and MOG. The numbers of M1 and M2 microglia/macrophage phenotypes present in the spinal cords of EAE-induced ngr1^＋/＋ and ngr1^–/– mice, were assessed by flow cytometric analysis using CD38 and Erg-2 markers. A significant difference in microglia/macrophage numbers between ngr1^＋/＋ and ngr1^–/– mice was identified during the progression of the clinical symptoms of EAE, in the white versus gray matter regions of the spinal cord. This difference was unrelated to the expression of Ng R on these macrophage/microglial cells. We have identified that as EAE progresses, the phagocytic activity of microglia/macrophages with myelin debris, in ngr1^–/– mice, was enhanced. Moreover, we show a modulation from a predominant M1-pathogenic to the M2-neurotrophic cell phenotype in the ngr1^–/– mice during EAE progression. These findings suggest that CNS-specific macrophages and microglia of ngr1^–/– mice may exhibit an enhanced capacity to clear inhibitory molecules that are sequestered in inflammatory lesions.展开更多
Dear Editor,Recent studies have emphasized the importance of editing cis-regulatory elements rather than protein-coding regions to subtly adjust plant traits(Rodrıguez-Leal et al.,2017).However,targeting cis-regulator...Dear Editor,Recent studies have emphasized the importance of editing cis-regulatory elements rather than protein-coding regions to subtly adjust plant traits(Rodrıguez-Leal et al.,2017).However,targeting cis-regulatory elements for mild phenotypic changes has been challenging,often failing to yield significant phenotypic change(Kwon et al.,2020).This underscores the necessity for innovative approaches to secure subtle phenotypic variations.Given the prevalence of gene duplication and redundancy in plant evolution,whereby multiple genes across different families may control a single function(Rodriguez-Leal et al.,2019),our approach involves editing several redundant genes within a family to precisely customize plant traits.展开更多
基金funded by National Research Foundation(NRF)of the Ministry of Science and ICT(MSIT),Republic of Korea(Grant Nos.2022R1C1C1002941,2020R1A2C1004273,2020R1A2C1101915)。
文摘Senescence,a crucial developmental process in the life cycle of plants,involves programmed destruction of cellular components of leaves.The onset of senescence is synchronized with other developmental processes for successful reproduction since senescence eventually leads to cell death.Arabinosyltransferase FASCIATED AND BRANCHED 2(FAB2)is known to control meristem proliferation.Here,we show that FAB2 could inhibit premature leaf senescence in tomato plants.Both chemically mutagenized and CRISPR-generated fab2 mutants exhibited excessively accelerated senescence,which resulted in sterility.Transcriptome analysis revealed that FAB2 extended leaf longevity by suppressing transcription of genes highly expressed in mature leaves.Transcription of FAB2 was increased in younger leaves,potentially inhibiting premature leaf senescence.The precocious senescence of fab2 mutants was in contrast to fasciated inflorescence(fin)mutants,which carried mutations in a hydroxyproline O-arabinosyltransferase gene,leading to meristem overproliferation.Our observations indicate that complex genetic hierarchy in the cascade of tomato arabinosyltransferases could control different aspects of developmental processes such as stem cell proliferation and senescence.
基金supported by Multiple Sclerosis Research Australia and Trish Multiple Sclerosis Research Foundation Postgraduate Scholarship(to JYL)the National Multiple Sclerosis Society Project Grant#RG4398A1/1+2 种基金International Progressive Multiple Sclerosis Alliance Challenge Award#PA0065Multiple Sclerosis Research Australia and Trish Multiple Sclerosis Research Foundation#15-022Bethlehem Griffiths Research Foundation#BGRF1706(to SP)
文摘Myelin-associated inhibitory factors within the central nervous system（CNS） are considered to be one of the main obstacles for axonal regeneration following disease or injury. The nogo receptor 1（NgR1） has been well documented to play a key role in limiting axonal regrowth in the injured and diseased mammalian CNS. However, the role of nogo receptor in immune cell activation during CNS inflammation is yet to be mechanistically elucidated. Microglia/macrophages are immune cells that are regarded as pathogenic contributors to inflammatory demyelinating lesions in multiple sclerosis（MS）. In this study, the animal model of MS, experimental autoimmune encephalomyelitis（EAE） was induced in ngr1^＋/＋ and ngr1^–/– female mice following injection with the myelin oligodendrocyte glycoprotein（MOG_（35–55）） peptide. A fatemap analysis of microglia/macrophages was performed throughout spinal cord sections of EAE-induced mice at clinical scores of 0, 1, 2 and 3, respectively（increasing locomotor disability） from both genotypes, using the CD11 b and Iba1 cell markers. Western immunoblotting using lysates from isolated spinal cord microglia/macrophages, along with immunohistochemistry and flow cytometric analysis, was performed to demonstrate the expression of nogo receptor and its two homologs during EAE progression. Myelin protein engulfment during EAE progression in ngr1^＋/＋ and ngr1^–/– mice was demonstrated by western immunblotting of lysates from isolated spinal cord microglia/macrophages, detecting levels of Nogo-A and MOG. The numbers of M1 and M2 microglia/macrophage phenotypes present in the spinal cords of EAE-induced ngr1^＋/＋ and ngr1^–/– mice, were assessed by flow cytometric analysis using CD38 and Erg-2 markers. A significant difference in microglia/macrophage numbers between ngr1^＋/＋ and ngr1^–/– mice was identified during the progression of the clinical symptoms of EAE, in the white versus gray matter regions of the spinal cord. This difference was unrelated to the expression of Ng R on these macrophage/microglial cells. We have identified that as EAE progresses, the phagocytic activity of microglia/macrophages with myelin debris, in ngr1^–/– mice, was enhanced. Moreover, we show a modulation from a predominant M1-pathogenic to the M2-neurotrophic cell phenotype in the ngr1^–/– mice during EAE progression. These findings suggest that CNS-specific macrophages and microglia of ngr1^–/– mice may exhibit an enhanced capacity to clear inhibitory molecules that are sequestered in inflammatory lesions.
基金funded by the National Research Foundation of Korea(NRF)grants fromthe Ministry of Science and ICT(MSIT),Republic of Korea(2022R1C1C1002941 and RS-2024-00407469 to C.-T.K.,2020R1A2C1101915 to S.J.P.,2020R1A2C1004273 to RS-2023-00217064 to W.-J.H.).
文摘Dear Editor,Recent studies have emphasized the importance of editing cis-regulatory elements rather than protein-coding regions to subtly adjust plant traits(Rodrıguez-Leal et al.,2017).However,targeting cis-regulatory elements for mild phenotypic changes has been challenging,often failing to yield significant phenotypic change(Kwon et al.,2020).This underscores the necessity for innovative approaches to secure subtle phenotypic variations.Given the prevalence of gene duplication and redundancy in plant evolution,whereby multiple genes across different families may control a single function(Rodriguez-Leal et al.,2019),our approach involves editing several redundant genes within a family to precisely customize plant traits.
