Type I phosphatidylinositol 4-phosphate 5-kinase isoforms are specifically stimulated by phosphatidic acid

Phospholipase D1 Ablation Disrupts Mouse Longitudinal Hippocampal Axis Organization and Functioning

“…Taking advantage of this property, Spo20p is regularly used as a PA probe and was found to co-localize with mammalian SNAP-25 in an experimental context of acutely activated exocytosis (Zeniou-Meyer et al, 2007). Moreover, SNAP-25 was reported to bind to anionic lipids, such as PA, and even though, to our knowledge, PA binding was not specifically tested, SNAP-25 was found to bind to PI(4,5)P 2 , which PA could still indirectly modulate by PIP5K activation (Jenkins et al, 1994;Stace et al, 2008). Although the reduction of SNAP-25 levels led to deficits in sociability behavior and susceptibility to pharmacologically induced seizures, it partially phenocopied Pld1 KO animals, which also show deficits in NOR and social interaction in a hippocampus-specific task (Figure 2) and no deficits in spatial learning and memory tasks (Corradini et al, 2014).…”

“…Since we observe here that PLD1 ablation reduces various lysoglycerophospholipid levels in the DH (Figure 1C), it further supports that PLA2 could be in a hypoactive state, partially explaining why LTD induction was reduced upon PLD1 ablation. Another possibility is based on the findings that PA binds and activates phosphatidylinositol 4-phosphate 5-kinase (PIP5K) (Jenkins et al, 1994;Stace et al, 2008), which was shown to be necessary for LFS LTD induction (Unoki et al, 2012). Moreover, since hippocalcin was shown to be necessary for LTD induction (Palmer et al, 2005) and to activate PLD (Hyun et al, 2000;Oh et al, 2006), these observations are coherent with a role for the PLD pathway in LTDassociated plasticity mechanisms, even if the contribution for each PLD isoenzyme should still be addressed.…”

Impaired degranulation but enhanced cytokine production after FcεRI stimulation of diacylglycerol kinase ζ–deficient mast cells

“…Additionally, PA itself is a second messenger, and DGK activity could regulate mast cell function by aff ecting PA accumulation. In vitro, PA is a potent activator of PLC and phosphatidylinositol 4-phosphate 5-kinase (PI5K), enzymes involved in PIP 2 degradation and production (35)(36)(37). Therefore, through conversion of DAG into PA, DGK enzymes could regulate many aspects of inositol lipid metabolism and mast cell activation after FcεRI engagement.…”

Expression and Localization of Type II Diacylglycerol Kinase Isozymes δ and η in the Developing Mouse Brain

“…In addition, they act as lipid second messengers in a wide variety of biological processes in mammalian cells (English 1996;Exton 1994;Hodgkin et al 1998). DG activates several signaling proteins, such as conventional protein kinase C (PKC), novel PKC, Unc-13, and Ras guanyl nucleotide-releasing protein (Hurley et al 1997;Nishizuka 1992;Ron and Kazanietz 1999), whereas PA regulates phosphatidylinositol-4-phosphate 5-kinase (Jenkins et al 1994;Moritz et al 1992), the mammalian targets of rapamycin (Fang et al 2001), and atypical PKC (Limatola et al 1994). Thus, DGK plays a pivotal role in various intracellular signaling pathways by regulating DG and PA concentrations.…”