abdominal segmentation defects of dAcsl mutants resemble those of gap gene knirps. The central expression domain of Kni transcripts or proteins is reduced whereas the adjacent domains of another gap gene Hunchback are correspondingly expanded in these mutants. Consequently, the striped pattern of the pair-rule gene Even-skipped is disrupted, phenotype, overview
lipid-induced up-regulation of acyl-CoA synthetase 5 promotes hepatocellular apoptosis. High ACSL5 activity results in enhanced caspase-3/7 activity, but is not accompanied by up-regulation of death receptors, DR4, DR5 or TNF-R1
loss of ACS-3, a long-chain acyl-CoA synthase, causes enhanced intestinal lipid uptake, de novo fat synthesis, and accumulation of enlarged, neutral lipid-rich intestinal depots. Acs-3 mutant phenotypes require the nuclear hormone receptor NHR-25, a key regulator of Caenorhabditis elegans molting
suppression of ACSL5 expression significantly decreases fatty acid-induced lipid droplet formation. ACSL5 knockdown results in decreased oleic acid or acetic acid incorporation into intracellular triacylglycerol, phospholipids, and cholesterol esters without altering fatty acid uptake or lipogenic gene expression. ACSL5 knockdown also decreases hepatic TAG secretion proportionate to the observed decrease in neutral lipid synthesis. ACSL5 knockdown does not alter lipid turnover or mediate the effects of insulin on lipid metabolism, phenotype, detailed overview
when compared to the wild-type strain, the fadD2 mutant exhibits decreased production of lipase, protease, rhamnolipid and phospholipase, and retardation of both swimming and swarming motilities. Interestingly, fadD1 mutant shows only increased swarming motility. Growth analysis of the fadD mutants show noticeable deficiencies in utilizing fatty acids and phosphatidylcholine as the sole carbon source, altered swimming and swarming motility of fadD mutants
knockdown of endogenous Acsl4 expression increases significantly the release of arachidonate metabolites, including prostaglandin E2, prostaglandin D2, and prostaglandin F2alpha, compared with replicated control cells, whereas knockdown of Acsl1 expression reduces the interleukin-1beta-induced release of arachidonate metabolites
dAcsl mutants exhibit neuromuscular junction (NMJ) overgrowth that is suppressed by reducing the doses of the bone morphogenetic protein, BMP, pathway components, accompanied by increased levels of activated BMP receptor Thickveins (Tkv) and phosphorylated mothers against decapentaplegic (Mad), the effector of the BMP signaling at NMJ terminals. In addition, Rab11, a small GTPase involved in endosomal recycling, is mislocalized in dAcsl mutant NMJs, and the membrane association of Rab11 is reduced in dAcsl mutant brains. The staining pattern of Rab11 is markedly alteredin dAcsl mutant NMJs, the abnormal Rab11 localization is specifically caused by dAcsl mutations. Consistently, the BMP receptor Tkv accumulates in early endosomes but is reduced in recycling endosomes in dAcsl mutant NMJs. The level of activated BMP receptor Tkv is elevated in dAcsl mutants. Phenotype, overview. The extended presynaptic distribution of Rab11 is completely reversed by both presynaptic and ubiquitous expression of human ACSL4
isoform ACSL6 genic inhibition in rat primary myotubes decreases lipid accumulation, as well as activates the higher mitochondrial oxidative capacity programme and fatty acid oxidation through the AMP-activated protein kinase/ peroxisome proliferator-activated receptor gamma coactivator 1-alpha pathway
acyl-CoA synthetase 5 is involved in the activation of long-chain fatty acids for lipid biosynthesis, and it is the only ACSL isoform that is both, located on mitochondria and functionally involved in enterocyte apoptosis. Analysis of regulation of ACSL5 in hepatocellular fatty acid degeneration and its involvement in hepatocyte apoptosis using models of in vitro and in vivo steatosis as well as plasmid-mediated stable gene transfer and RNAi-mediated gene silencing
acyl-CoA synthetase 5 plays a key role in fatty acid metabolism. Isoform ACSL5 plays a role in channelling fatty acids towards palmitoylation and other lipid functions with high relevance for cellular behaviour
long chain acyl CoA synthetase 4 is a key enzyme in steroidogenesis. It participates in steroid synthesis through of arachidonic acid release and steroidogenic acute regulatory protein induction
the expression of FATP2 slightly, but reproducibly, increases both C16:0-CoA and C20:4-CoA derived from exogenous fatty acids, the formation of acyl CoA from C18:3 and C22:6 is significant
dAcsl is the Drosophila homolog of human ACSL4 and their functions are highly conserved in the processes ranging from lipid metabolism to the establishment of visual wiring, both maternal and zygotic dAcsl are required for embryonic segmentation
FACL3 is a critical enzyme for activation of long-chain fatty acids. FACL3-mediated 1alpha,25(OH)2D3 inhibition of fatty acid synthase is associated with many cancers, including prostate cancer
isozyme LACS9 is the major LACS isoform involved in plastidial fatty acid export for triacylglycerol formation. Isozymes LACS1 and LACS9 have overlapping functions in triacylglycerol biosynthesis. LACS1 is localized in the endoplasmic reticulum and is involved in cuticular lipid synthesis
regulation of Caenorhabditis elegans fat uptake and storage by acyl-CoA synthase-3 is dependent on NR5A family nuclear hormone receptor nhr-25, overview. ACS-3-derived long-chain fatty acyl-CoAs, perhaps incorporated into complex ligands such as phosphoinositides, modulate NHR-25 function, which in turn regulates an endocrine program of lipid uptake and synthesis
Acsl isozymes play distinct roles in the control of arachidonate remodeling in rat fibroblasts: isoform Acsl4 acts as the first step of enzyme for arachidonate remodeling following interleukin-1beta stimulation, and isoform Acsl1 is involved in the maintenance of some arachidonate-containing phosphatidylcholine species
Arabidopsis long-chain acyl-CoA synthetase isoforms LACS1, LACS2, and LACS3 facilitate fatty acid uptake in yeast. Expression of each isoform in yeast results in uptake of the long-chain fatty acid analogue, C1-Bodipy-C12. Only expression of LACS1 results in uptake of the very-long-chain fatty acid analogue, Bodipy-C16
ACSL4 regulates neural development, role of ACSL4 in endosomal trafficking in vivo. ACSL4 is highly expressed in the hippocampus, a structure critical for learning and memory. Recombinant expression of human ACSL4 rescues the endocytic trafficking and neuromuscular junction (NMJ) phenotypes of Drosophila melanogaster enzyme mutants of the homologue dAcsl. The extended presynaptic distribution of Rab11 is completely reversed by both presynaptic and ubiquitous expression of human ACSL4
dAcsl, the Drosophila orthologue of ACSL4 and ACSL3, inhibits synaptic growth by attenuating bone morphogenetic protein, BMP, signaling, a major growth-promoting pathway at neuromuscular junction (NMJ) synapses. dAcsl is also required for the recycling of photoreceptor rhodopsin in the eyes, implying a general role for dAcsl in regulating endocytic recycling of membrane receptors, dAcsl promotes rhodopsin recycling in photoreceptors, dAcsl inhibits endocytosis of BMP receptors. dAcsl regulates the membrane distribution of Rab11 at NMJs. dAcsl genetically interacts with rab11 in attenuating BMP signaling at NMJ synapses through facilitating Rab11 dependent BMP receptor recycling
isoform Acsl1 overexpression prevents oxidative stress (nitrotyrosine, hydroxyoctadecadienoic acids) and attenuates cellular injury in Schwann cells following 12 h exposure to long chain fatty acids
upregulation of isoform ACSL4 is responsible for the increase in polyunsaturated fatty acid-triacylglycerol species during activation of hepatic stellate cells, which may serve to protect cells against a shortage of polyunsaturated fatty acids required for eicosanoid secretion
Aspergillus nidulans contains six possible fatty acyl-CoA synthetases with FaaB being the major synthetase for fatty acid degradation. Deletion of faaB leads to growth defects on fatty acids but does not affect the induction of genes involved in boxidation
lacs9 null mutant do not show any detectable phenotype. Disruption of LACS8 in the lacs8 mutant and lacs8 lacs9 double mutant, and over-expression of LACS8, do not affect the seed fatty acid content
long-chain acyl-CoA synthetase member 6, ASCL6, is a form present in the plasma membrane of cells. Splicing events affecting the N-terminus and alternative motifs near the ATP-binding site generate different isoforms of ACSL6. Alternative fatty acid Gate-domain motifs are essential determinants for the activity of the human ACSL6 isoforms, which appear to act as homodimeric enzyme as well as in complex with other spliced forms. The diversity of these enzyme species can produce the variety of acyl-CoA synthetase activities that are necessary to generate and repair the hundreds of lipid species present in membranes. Oligomeric complex fomations and interactions between isoforms, overview. The N-terminal domain is not essential for oligomer formation