Archives

  • 2018-07
  • 2018-10
  • 2018-11
  • 2019-04
  • 2019-05
  • 2019-06
  • 2019-07
  • 2019-08
  • 2019-09
  • 2019-10
  • 2019-11
  • 2019-12
  • 2020-01
  • 2020-02
  • 2020-03
  • 2020-04
  • 2020-05
  • 2020-06
  • 2020-07
  • 2020-08
  • 2020-09
  • 2020-10
  • 2020-11
  • 2020-12
  • 2021-01
  • 2021-02
  • 2021-03
  • 2021-04
  • 2021-05
  • 2021-06
  • 2021-07
  • 2021-08
  • 2021-09
  • 2021-10
  • 2021-11
  • 2021-12
  • 2022-01
  • 2022-02
  • 2022-03
  • 2022-04
  • 2022-05
  • 2022-06
  • 2022-07
  • 2022-08
  • 2022-09
  • 2022-10
  • 2022-11
  • 2022-12
  • 2023-01
  • 2023-02
  • 2023-03
  • 2023-04
  • 2023-05
  • 2023-06
  • 2023-07
  • 2023-08
  • 2023-09
  • 2023-10
  • 2023-11
  • 2023-12
  • 2024-01
  • 2024-02
  • 2024-03
  • 2024-04
  • In bacteria H gler et al Kanao et

    2024-02-23

    In bacteria (Hügler et al., 2007, Kanao et al., 2001), a glaucophyte alga (Ma et al., 2001), green algae/land plants (Fatland et al., 2002), and filamentous fungi (Nowrousian et al., 2000), ACL enzyme activity requires ACLA, and ACLB (referred to here as dual-subunit ACL, or dsACL) (Kanao et al., 2001). ACLA is homologous to the β subunit of succinyl-CoA synthetase (SCS), while ACLB is homologous to the α subunit of SCS, fused to a small portion homologous to citrate synthase (CS). An evolutionary model for the origin of ACL from the aforementioned TCA nor-NOHA acetate enzymes via gene duplication, fusion, and divergence has been suggested (Fatland et al., 2002). In contrast, animal ACL is a fusion protein (referred to here as single-subunit ACL, or ssACL) (Elshourbagy et al., 1990, Elshourbagy et al., 1992); the N-terminal portion is homologous to ACLA, and the C-terminal portion to ACLB. It was suggested that ssACL represents a molecular synapomorphy of animals (Fatland et al., 2002), although ssACL homologs were recently identified in some non-ascomycete fungi (Hynes and Murray, 2010). Here, we have undertaken a comprehensive phylogenetic analysis of ACL across eukaryotes. We demonstrate that ssACL and dsACL constitute ancient, distinct monophyletic lineages, that dsACL and ssACL have been laterally transferred and lost numerous times, and, contrary to previous analyses, that ssACL is likely the product of a gene fusion event that occurred very early in eukaryotic evolution.
    Methods
    Results and discussion
    Conclusions As sequence data accumulate, more prokaryote-derived gene fusions are being identified in eukaryotic nuclear genomes (Gawryluk et al., 2014, Maguire et al., 2014, Stairs et al., 2014, Stechmann and Cavalier-Smith, 2002); in many cases, these genes derive from relatively recent transfer/fusion events. In contrast, we have demonstrated here that the fusion of ACLA and ACLB into ssACL is not a curious feature of animals; rather ssACL, along with dsACL, likely represents an ancestral feature of eukaryotic genomes. Our phylogenetic analyses demonstrate that the evolution of ACL in eukaryotes has involved vertical inheritance, LGT, extensive gene loss, and gene fusion/fission. Moreover, these results emphasize the insidiousness of homoplasy in supposedly rare genomic changes (Maguire et al., 2014), and how the propensity to overstate the importance of such characters (Stechmann and Cavalier-Smith, 2002) may ultimately impair the interpretation of evolutionary relationships.
    Acknowledgments LE was supported by a CGEB postdoctoral fellowship from the Tula Foundation. RMRG’s postdoctoral fellowship and this work were supported by a CIHR-NSHRF RPP Grant (FRN# 62809) awarded to AJR.
    Introduction Dysregulation in mitochondrial oxidative phosphorylation (OXPHOS) as well as mitochondrial complex activity is associated with various skeletal muscle pathologies, including cachexia, sarcopenia, and the muscular dystrophies (Julienne et al., 2012, Marzetti et al., 2013, Szendroedi et al., 2008, Wang et al., 2010, White et al., 2011). Mitochondrial complexes are organized into several supercomplexes that facilitate the flow of electrons and thus make the system more efficient, minimizing ROS generation (Lapuente-Brun et al., 2013). It was also speculated that complex stability is influenced by the organization of supercomplexes. Recently, Ikeda et al. showed that mitochondrial activity is impaired and ATP content decreased by lack of supercomplex formation (Ikeda et al., 2013). Anabolic stimuli like exercise have a positive impact on skeletal muscle strength, endurance, and aerobic capacity by increasing protein synthesis, in addition to mitochondrial and contractile function of skeletal muscle (Egan and Zierath, 2013, Egerman and Glass, 2014, Riedl et al., 2010). The positive effects of exercise extend to diseased populations and to the elderly (Fiatarone et al., 1990, Hansen et al., 2010, Jeppesen et al., 2006). Some of these effects are elicited in response to contractile activity and mediated by anabolic factors such as insulin growth factor 1 (IGF1) (Schiaffino et al., 2013).