start-ver=1.4 cd-journal=joma no-vol=149 cd-vols= no-issue=8 article-no= start-page=dev199916 end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=2021 dt-pub=20211109 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Toll signalling promotes blastema cell proliferation during cricket leg regeneration via insect macrophages en-subtitle= kn-subtitle= en-abstract= kn-abstract=Hemimetabolous insects, such as the two-spotted cricket Gryllus bimaculatus, can recover lost tissues, in contrast to the limited regenerative abilities of human tissues. Following cricket leg amputation, the wound surface is covered by the wound epidermis, and plasmatocytes, which are insect macrophages, accumulate in the wound region. Here, we studied the function of Toll-related molecules identified by comparative RNA sequencing during leg regeneration. Of the 11 Toll genes in the Gryllus genome, expression of Toll2-1, Toll2-2 and Toll2-5 was upregulated during regeneration. RNA interference (RNAi) of Toll, Toll2-1, Toll2-2, Toll2-3 or Toll2-4 produced regeneration defects in more than 50% of crickets. RNAi of Toll2-2 led to a decrease in the ratio of S- and M-phase cells, reduced expression of JAK/STAT signalling genes, and reduced accumulation of plasmatocytes in the blastema. Depletion of plasmatocytes in crickets using clodronate also produced regeneration defects, as well as fewer proliferating cells in the regenerating legs. Plasmatocyte depletion also downregulated the expression of Toll and JAK/STAT signalling genes in the regenerating legs. These results suggest that Spz-Toll-related signalling in plasmatocytes promotes leg regeneration through blastema cell proliferation by regulating the Upd-JAK/STAT signalling pathway. en-copyright= kn-copyright= en-aut-name=BandoTetsuya en-aut-sei=Bando en-aut-mei=Tetsuya kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=OkumuraMisa en-aut-sei=Okumura en-aut-mei=Misa kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=BandoYuki en-aut-sei=Bando en-aut-mei=Yuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=HagiwaraMarou en-aut-sei=Hagiwara en-aut-mei=Marou kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=HamadaYoshimasa en-aut-sei=Hamada en-aut-mei=Yoshimasa kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=IshimaruYoshiyasu en-aut-sei=Ishimaru en-aut-mei=Yoshiyasu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=MitoTaro en-aut-sei=Mito en-aut-mei=Taro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=KawaguchiEri en-aut-sei=Kawaguchi en-aut-mei=Eri kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=InoueTakeshi en-aut-sei=Inoue en-aut-mei=Takeshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=AgataKiyokazu en-aut-sei=Agata en-aut-mei=Kiyokazu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= en-aut-name=NojiSumihare en-aut-sei=Noji en-aut-mei=Sumihare kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=11 ORCID= en-aut-name=OhuchiHideyo en-aut-sei=Ohuchi en-aut-mei=Hideyo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=12 ORCID= affil-num=1 en-affil=Department of Cytology and Histology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=2 en-affil=Department of Cytology and Histology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=3 en-affil=Faculty of Medicine, Okayama University Medical School kn-affil= affil-num=4 en-affil=Faculty of Medicine, Okayama University Medical School kn-affil= affil-num=5 en-affil=Department of Cytology and Histology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=6 en-affil=Division of Bioscience and Bioindustry, Graduate School of Technology, Industrial and Social Sciences, Tokushima University kn-affil= affil-num=7 en-affil=Division of Bioscience and Bioindustry, Graduate School of Technology, Industrial and Social Sciences, Tokushima University kn-affil= affil-num=8 en-affil=Division of Biological Science, Graduate School of Science, Kyoto University kn-affil= affil-num=9 en-affil=Division of Biological Science, Graduate School of Science, Kyoto University kn-affil= affil-num=10 en-affil=Division of Biological Science, Graduate School of Science, Kyoto University kn-affil= affil-num=11 en-affil=Division of Bioscience and Bioindustry, Graduate School of Technology, Industrial and Social Sciences, Tokushima University kn-affil= affil-num=12 en-affil=Department of Cytology and Histology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= en-keyword=Regeneration kn-keyword=Regeneration en-keyword=Toll-related signalling kn-keyword=Toll-related signalling en-keyword=JAK/STAT signalling kn-keyword=JAK/STAT signalling en-keyword=Macrophages kn-keyword=Macrophages en-keyword=Blastema kn-keyword=Blastema en-keyword=Gryllus bimaculatus kn-keyword=Gryllus bimaculatus END start-ver=1.4 cd-journal=joma no-vol=131 cd-vols= no-issue=7 article-no= start-page=1619 end-page=1628 dt-received= dt-revised= dt-accepted= dt-pub-year=2004 dt-pub=200404 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Collagen IV is essential for basement membrane stability but dispensable for initiation of its assembly during early development en-subtitle= kn-subtitle= en-abstract= kn-abstract=Basement membranes are specialized extracellular matrices consisting of tissue-specific organizations of multiple matrix molecules and serve as structural barriers as well as substrates for cellular interactions. The network of collagen IV is thought to define the scaffold integrating other components such as, laminins, nidogens or perlecan, into highly organized supramolecular architectures. To analyze the functional roles of the major collagen IV isoform ƒ¿1(IV 2ƒ¿2(IV) for basement membrane assembly and embryonic development, we generated a null allele of the Col4a1/2 locus in mice, thereby ablating both ƒ¿-chains. Unexpectedly, embryos developed up to E9.5 at the expected Mendelian ratio and showed a variable degree of growth retardation. Basement membrane proteins were deposited and assembled at expected sites in mutant embryos, indicating that this isoform is dispensable for matrix deposition and assembly during early development. However, lethality occurred between E10.5-E11.5, because of structural deficiencies in the basement membranes and finally by failure of the integrity of Reichert's membrane. These data demonstrate for the first time that collagen IV is fundamental for the maintenance of integrity and function of basement membranes under conditions of increasing mechanical demands, but dispensable for deposition and initial assembly of components. Taken together with other basement membrane protein knockouts, these data suggest that laminin is sufficient for basement membrane-like matrices during early development, but at later stages the specific composition of components including collagen IV defines integrity, stability and functionality. en-copyright= kn-copyright= en-aut-name=P?schlErnst en-aut-sei=P?schl en-aut-mei=Ernst kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=Schl?tzer-SchrehardtUrsula en-aut-sei=Schl?tzer-Schrehardt en-aut-mei=Ursula kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=BrachvogelBent en-aut-sei=Brachvogel en-aut-mei=Bent kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=SaitoKenji en-aut-sei=Saito en-aut-mei=Kenji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=NinomiyaYoshifumi en-aut-sei=Ninomiya en-aut-mei=Yoshifumi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=MayerUlrike en-aut-sei=Mayer en-aut-mei=Ulrike kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= affil-num=1 en-affil= kn-affil=Department of Experimental Medicine I, University Erlangen-N?rnberg affil-num=2 en-affil= kn-affil=Department of Ophthalmology, University Erlangen-N?rnberg affil-num=3 en-affil= kn-affil=Department of Experimental Medicine I, University Erlangen-N?rnberg affil-num=4 en-affil= kn-affil=Department of Molecular Biology and Biochemistry, Okayama University Medical School affil-num=5 en-affil= kn-affil=Department of Molecular Biology and Biochemistry, Okayama University Medical School affil-num=6 en-affil= kn-affil=Wellcome Trust Centre for Cell-Matrix Research, School of Biological Sciences, University of Manchester en-keyword=Collagen IV kn-keyword=Collagen IV en-keyword=Col4a1 kn-keyword=Col4a1 en-keyword=Col4a2 kn-keyword=Col4a2 en-keyword=Knockout kn-keyword=Knockout en-keyword=Basement kn-keyword=Basement en-keyword=membrane kn-keyword=membrane en-keyword=Development kn-keyword=Development END start-ver=1.4 cd-journal=joma no-vol=133 cd-vols= no-issue=18 article-no= start-page=3575 end-page=3585 dt-received= dt-revised= dt-accepted= dt-pub-year=2006 dt-pub=20060915 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=The dwarf phenotype of the Arabidopsis acl5 mutant is suppressed by a mutation in an upstream ORF of a bHLH gene en-subtitle= kn-subtitle= en-abstract= kn-abstract=Loss-of-function mutants of the Arabidopsis thaliana ACAULIS 5 (ACL5) gene, which encodes spermine synthase, exhibit a severe dwarf phenotype. To elucidate the ACL5-mediated regulatory pathways of stem internocle elongation, we isolated four suppressor of acaulis (sac) mutants that reverse the acl5 dwarf phenotype. Because these mutants do not rescue the dwarfism of known phytohormone-related mutants, the SAC genes appear to act specifically on the ACL5 pathways. We identify the gene responsible for the dominant sac51-d mutant, which almost completely suppresses the acl5 phenotype. sac51-d disrupts a short upstream open reading frame (uORF) of SAC51, which encodes a bHLH-type transcription factor. Our results indicate that premature termination of the uORF in sac51-d results in an increase in its own transcript level, probably as a result of an increased translation of the main ORF. We suggest a model in which ACL5 plays a role in the translational activation of SAC51, which may lead to the expression of a subset of genes required for stem elongation. en-copyright= kn-copyright= en-aut-name=ImaiAkihiro en-aut-sei=Imai en-aut-mei=Akihiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=HanzawaYoshie en-aut-sei=Hanzawa en-aut-mei=Yoshie kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=KomuraMio en-aut-sei=Komura en-aut-mei=Mio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=YamamotoKotaro T. en-aut-sei=Yamamoto en-aut-mei=Kotaro T. kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=KomedaYoshibumi en-aut-sei=Komeda en-aut-mei=Yoshibumi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=TakahashiTaku en-aut-sei=Takahashi en-aut-mei=Taku kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= affil-num=1 en-affil= kn-affil=Division of Bioscience, Graduate School of Natural Science and Technology, Okayama University affil-num=2 en-affil= kn-affil=Division of Biological Sciences, Graduate School of Science, Hokkaido University affil-num=3 en-affil= kn-affil=Division of Bioscience, Graduate School of Natural Science and Technology, Okayama University affil-num=4 en-affil= kn-affil=Division of Biological Sciences, Graduate School of Science, Hokkaido University affil-num=5 en-affil= kn-affil=Division of Biological Sciences, Graduate School of Science, Hokkaido University affil-num=6 en-affil= kn-affil=Division of Bioscience, Graduate School of Natural Science and Technology, Okayama University en-keyword=Arabidopsis thaliana kn-keyword=Arabidopsis thaliana en-keyword=Polyamine kn-keyword=Polyamine en-keyword=Spermine kn-keyword=Spermine en-keyword=Stem elongation kn-keyword=Stem elongation en-keyword=Upstream ORF kn-keyword=Upstream ORF END