Hengartner MO (1997) Nature "Apoptosis. CED-4 is a stranger no more."

Hengartner MO

[Nature, 1997]

The nematode worm Caenorhabditis elegans has been used with great success to identify the basic components of the machinery underlying apoptosis (programmed cell death). Indeed, of the three key cell death genes that have been identified in C. elegans, two - ced-3 and ced-9 - have mammalian homologues that also function in apoptosis. But the sequence of the third gene, ced-4, revealed no obvious mammalian homologue, and precious little in terms of possible mechanism of action. A flurry of activity has changed that. A paper by Zou et al., published earlier this month in Cell, provides a homologue. And work by Chinnaiyan et al. (page 728 of this issue) and by Seshagiri and Miller in Current Biology lays down some choreography for the part that CED-4 protein plays in the molecular dance of death.

Levine MS et al. (2014) Structure "Polo-like kinase 4 shapes up."

Holland AJ, Levine MS

[Structure, 2014]

Polo-like kinase 4 (Plk4) is a master regulator of centriole duplication and targets to centrioles through the association of its cryptic polo box domain with centriole receptors. In this issue of Structure, Shimanovskaya and colleagues unveil a new dimeric architecture of Plk4's cryptic polo box that reveals a conserved mechanism for centriole targeting of the kinase.

Van Voorhies WA (2001) Hum Exp Toxicol "Hormesis and aging."

Van Voorhies WA

[Hum Exp Toxicol, 2001]

Rattan?s article on the potential use of hormesis in aging research provides a well-reasoned and insightful overview of both the factors responsible for aging and the importance of stress responses in potentially modulating senescence. Rattan proceeds from the premise that the causal mechanisms responsible for aging are likely to vary not only between, and within species, but also even between different cell types of the same individual. As such, aging may have different causal mechanisms between different species, and multiple causal mechanisms within species. As a direct consequence of this, it is unlikely that a single cause of aging will be common to all

Lackner MR et al. (1999) Neuron "Facilitation of synaptic transmission by EGL-30 Gqalpha and EGL-8 PLCbeta: DAG binding to UNC-13 is required to stimulate acetylcholine release."

Lackner MR, Nurrish SJ, Kaplan JM

[Neuron, 1999]

We show that neurotransmitter release at Caenorhabditis elegans neuromuscular junctions is facilitated by a presynaptic pathway composed of a Gqalpha (EGL-30), EGL-8 phospholipase Cbeta (PLCbeta), and the diacylglycerol- (DAG-) binding protein UNC-13. Activation of this pathway increased release of acetylcholine at neuromuscular junctions, whereas inactivation decreased release. Phorbol esters stimulated acetylcholine release, and this effect was blocked by a mutation that eliminates phorbol ester binding to UNC-13. Expression of a constitutively membrane-bound form of UNC-13 restored acetylcholine release to mutants lacking the egl-8 PLCbeta. Activation of this pathway with muscarinic agonists caused UNC-13 to accumulate in punctate structures in the ventral nerve cord. These results suggest that presynaptic DAG facilitates synaptic transmission and that part of this effect is mediated by UNC-13.AD - Department of Molecular and Cell Biology, University of California, Berkeley 94720, USA.FAU - Lackner, M RAU - Lackner MRFAU - Nurrish, S JAU - Nurrish SJFAU - Kaplan, J MAU - Kaplan JMLA - engID - GM54728/GM/NIGMSPT - Journal ArticleCY - UNITED STATESTA - NeuronJID - 8809320RN - 0 (Diglycerides)RN - 0 (Helminth Proteins)RN - 0 (Isoenzymes)RN - 0 (Muscarinic Agonists)RN - 0 (Unc-13 protein)RN - 16561-29-8 (Tetradecanoylphorbol Acetate)RN - 51-84-3 (Acetylcholine)RN - EC 3.1.4.- (phospholipase C beta)RN - EC 3.1.4.3 (Phospholipase C)RN - EC 3.6.1.- (GTP-Binding Proteins)SB - IM