Essential for plant growth, promotes cell division in root meristems (PubMed:21666002, PubMed:21883234, PubMed:26276842). Catalyzes the biosynthesis of ceramide sphingolipids with C(16) to C(28) fatty acids, structural membrane lipids involved in membrane trafficking (e.g. early endosomes) and cell polarity (e.g. polar auxin transport related proteins); active on a broad substrate spectrum, both regarding chain lengths of fatty acids and the sphingoid base, such as long-chain base (LCB) phytosphingosine (t18:0) (PubMed:21883234, PubMed:26635357, PubMed:21666002, PubMed:26276842). Mediates resistance to sphinganine-analog mycotoxins (SAMs, e.g. fumonisin B(1)) by restoring the sphingolipid biosynthesis (PubMed:26276842). Could salvage the transport of GPI-anchored proteins from the endoplasmic reticulum to the Golgi apparatus in ceramides-depleted cells after SAM exposure (By similarity). Contributes to hypoxic conditions tolerance (e.g. submergences), especially in the dark, by promoting the formation of very-long-chain (VLC) ceramide species (22:1, 24:1 and 26:1) and of VLC unsaturated ceramides, which are modulating CTR1-mediated ethylene signaling leading to endoplasmic reticulum (ER)-to-nucleus translocation of EIN2 and EIN3 (PubMed:25822663). (4R)-hydroxysphinganine + a fatty acyl-CoA = an N-acyl-(4R)-4-hydroxysphinganine + CoA + H(+) a sphingoid base + tetracosanoyl-CoA = an N-tetracosanoyl-sphingoid base + CoA + H(+) (4R)-hydroxysphinganine + hexadecanoyl-CoA = CoA + H(+) + N-hexadecanoyl-(4R)-hydroxysphinganine (4R)-hydroxysphinganine + octadecanoyl-CoA = CoA + H(+) + N-octadecanoyl-(4R)-hydroxysphinganine (4R)-hydroxysphinganine + eicosanoyl-CoA = CoA + H(+) + N-eicosanoyl-(4R)-hydroxysphinganine (4R)-hydroxysphinganine + docosanoyl-CoA = CoA + H(+) + N-docosanoyl-(4R)-hydroxysphinganine (4R)-hydroxysphinganine + hexacosanoyl-CoA = CoA + H(+) + N-hexacosanoyl-(4R)-hydroxysphinganine (4R)-hydroxysphinganine + tetracosanoyl-CoA = CoA + H(+) + N-tetracosanoyl-(4R)-hydroxysphinganine sphing-4-enine + tetracosanoyl-CoA = CoA + H(+) + N-tetracosanoyl-sphing-4-enine sphinga-(4E,8Z)-dienine + tetracosanoyl-CoA = CoA + H(+) + N-tetracosanoylsphinga-(4E,8Z)-dienine sphinga-(4E,8E)-dienine + tetracosanoyl-CoA = CoA + H(+) + N-tetracosanoylsphinga-(4E,8E)-dienine (4R)-hydroxysphing-(8Z)-enine + tetracosanoyl-CoA = CoA + H(+) + N-tetracosanoyl-(4R)-hydroxysphing-(8Z)-enine (4R)-hydroxysphing-(8E)-enine + tetracosanoyl-CoA = CoA + H(+) + N-tetracosanoyl-(4R)-hydroxysphing-(8E)-enine Inhibited by the mycotoxin fumonisin B(1), a sphingosine analog mycotoxins produced by pathogenic fungi (PubMed:26276842, PubMed:26635357). Repressed by divalent cation such as magnesium Mg(2+), copper Cu(2+), zinc Zn(2+), manganese Mn(2+), calcium Ca(2+) and cobalt Co(2+) (PubMed:26635357). Sphingolipid metabolism. Expressed ubiquitously at low levels (PubMed:21883234). Not observed in pollen (PubMed:25794895). No visible impact on ceramide and glucosylceramide species with C(14) to C(28) fatty acids (PubMed:21883234). The double mutant loh1 loh3 is embryonically lethal (PubMed:21883234, PubMed:21666002). Rare viable loh1 loh3 seedlings have a complete absence of very-long-chain fatty acid (VLCFA) in sphingolipids and exhibit strong dwarf phenotype and altered lateral root outgrowth associated with disrupted early endosomes and an impaired polar auxin transport due to abnormal localization of auxin transporters in the plasma membrane; these phenotypes are in part restored by external auxin (NAA) (PubMed:21666002). Better resistance to submergence under light conditions, but increased sensitivity to dark submergence associated with declined levels of unsaturated very-long-chain (VLC) ceramide species (22:1, 24:1 and 26:1) (PubMed:25822663). The double mutant loh1 loh3, lacking (VLC) ceramides, have an impaired tolerance to both dark and light submergences (PubMed:25822663). May be due to intron retention.