Expression in yeast of an acyl-CoA:diacylglycerol acyltransferase cDNA from Caenorhabditis elegans

2000 ◽  
Vol 28 (6) ◽  
pp. 692-695 ◽  
Author(s):  
P. Bouvier-Navé ◽  
P. Benveniste ◽  
A. Noiriel ◽  
H. Schaller

we have identified a cDNA from the nematode worm Caenorhabditis elegans that encodes an acyl-CoA: diacylglycerol acyltransferase (DGAT). Its expression in Saccharomyces cerevisiae resulted in an increase both in triacylglycerol content and in microsomal oleyl-CoA: diacylglycerol acyltransferase activity. Such effects were similar to those of characterized plant DGAT genes. This is the first DGAT gene isolated from an invertebrate. The phylogenetic relationships between DGATs and animal and yeast acyl-CoA: sterol acyltransferases are illustrated.

2021 ◽  
Author(s):  
Robert Friedman

The nematode worm, Caenorhabditis elegans, is a relatively simple neural system model for measuring the efficiency of information transmission from sensory organ to muscle fiber. With the potential to measure this efficiency, a method is proposed to compare the organization of an idealized neural circuit with a logic gate design. This approach is useful for analysis of a neural circuit that is not tractable to a strictly biological model, and where the assumptions of a logic gate design have applicability. Also, included in the results is an abstract perspective of the electrical-specific synaptic network in the somatic system of the nematode worm.


DNA Sequence ◽  
1994 ◽  
Vol 4 (5) ◽  
pp. 281-291 ◽  
Author(s):  
Michael J. Runswick ◽  
Alexander Philippides ◽  
Graziantonio Lauria ◽  
John E. Walker

1987 ◽  
Vol 245 (1) ◽  
pp. 257-261 ◽  
Author(s):  
L A Meheus ◽  
J J Van Beeumen ◽  
A V Coomans ◽  
J R Vanfleteren

The nematode worm Caenorhabditis elegans is known to undergo characteristic morphological as well as physiological signs of senescence. Two-dimensional gel electrophoresis shows that alterations also occur in the pattern of the nuclear proteins as a function of age. Non-histone proteins whose level exhibits a steep fall with age are egg-specific and not involved in senescence. However, a distinct set of non-histones accumulates with age and can be considered as senescence markers. Some of these are glycoproteins, as shown by their concanavalin A-binding properties. One age-specific polypeptide, called ‘protein S-28’, was further characterized by peptide mapping and determination of its N-terminal amino acid sequence.


2007 ◽  
Vol 408 (1) ◽  
pp. 61-68 ◽  
Author(s):  
Yasushi Kamisaka ◽  
Nao Tomita ◽  
Kazuyoshi Kimura ◽  
Kumiko Kainou ◽  
Hiroshi Uemura

We previously found that SNF2, a gene encoding a transcription factor forming part of the SWI/SNF (switching/sucrose non-fermenting) chromatin-remodelling complex, is involved in lipid accumulation, because the Δsnf2 disruptant of Saccharomyces cerevisiae has a higher lipid content. The present study was conducted to identify other factors that might further increase lipid accumulation in the Δsnf2 disruptant. First, expression of LEU2 (a gene encoding β-isopropylmalate dehydrogenase), which was used to select transformed strains by complementation of the leucine axotroph, unexpectedly increased both growth and lipid accumulation, especially in the Δsnf2 disruptant. The effect of LEU2 expression on growth and lipid accumulation could be reproduced by adding large amounts of leucine to the culture medium, indicating that the effect was not due to Leu2p (β-isopropylmalate dehydrogenase) itself, but rather to leucine biosynthesis. To increase lipid accumulation further, genes encoding the triacylglycerol biosynthetic enzymes diacylglycerol acyltransferase (DGA1) and phospholipid:diacylglycerol acyltransferase (LRO1) were overexpressed in the Δsnf2 disruptant. Overexpression of DGA1 significantly increased lipid accumulation, especially in the Δsnf2 disruptant, whereas LRO1 overexpression decreased lipid accumulation in the Δsnf2 disruptant. Furthermore, the effect of overexpression of acyl-CoA synthase genes (FAA1, FAA2, FAA3 and FAA4), which each supply a substrate for Dga1p (diacylglycerol acyltransferase), was investigated. Overexpression of FAA3, together with that of DGA1, did not further increase lipid accumulation in the Δsnf2 disruptant, but did enhance lipid accumulation in the presence of exogenous fatty acids. Lastly, the total lipid content in the Δsnf2 disruptant transformed with DGA1 and FAA3 overexpression vectors reached approx. 30%, of which triacylglycerol was the most abundant lipid. Diacylglycerol acyltransferase activity was significantly increased in the Δsnf2 disruptant strain overexpressing DGA1 as compared with the wild-type strain overexpressing DGA1; this higher activity may account for the prominent increase in lipid accumulation in the Δsnf2 disruptant with DGA1 overexpression. The strains obtained have a lipid content that is high enough to act as a model of oleaginous yeast and they may be useful for the metabolic engineering of lipid production in yeast.


2001 ◽  
Vol 122 (13) ◽  
pp. 1477-1495 ◽  
Author(s):  
Anatoli I. Yashin ◽  
James R. Cypser ◽  
Thomas E. Johnson ◽  
Anatoli I. Michalski ◽  
Sergei I. Boyko ◽  
...  

2001 ◽  
Vol 37 (1) ◽  
pp. 57-66 ◽  
Author(s):  
Alexander Butov ◽  
Thomas Johnson ◽  
James Cypser ◽  
Igor Sannikov ◽  
Maxim Volkov ◽  
...  

Genetics ◽  
2021 ◽  
Author(s):  
Bhavya Ravi ◽  
Jian Zhao ◽  
I Chaudhry ◽  
Rossana Signorelli ◽  
Mattingly Bartole ◽  
...  

Abstract Egg laying in the nematode worm Caenorhabditis elegans is a two-state behavior modulated by internal and external sensory input. We have previously shown that homeostatic feedback of embryo accumulation in the uterus regulates bursting activity of the serotonergic HSN command neurons that sustains the egg-laying active state. How sensory feedback of egg release signals to terminate the egg-laying active state is less understood. We find that Gαo, a conserved Pertussis Toxin-sensitive G protein, signals within HSN to inhibit egg-laying circuit activity and prevent entry into the active state. Gαo signaling hyperpolarizes HSN, reducing HSN Ca2+ activity and input onto the postsynaptic vulval muscles. Loss of inhibitory Gαo signaling uncouples presynaptic HSN activity from a postsynaptic, stretch-dependent homeostat, causing precocious entry into the egg-laying active state when only a few eggs are present in the uterus. Feedback of vulval opening and egg release activates the uv1 neuroendocrine cells which release NLP-7 neuropeptides which signal to inhibit egg laying through Gαo-independent mechanisms in the HSNs and Gαo-dependent mechanisms in cells other than the HSNs. Thus, neuropeptide and inhibitory Gαo signaling maintains a bi-stable state of electrical excitability that dynamically controls circuit activity in response to both external and internal sensory input to drive a two-state behavior output.


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