Abstracts - faqs.org

Abstracts

Biological sciences

Search abstracts:
Abstracts » Biological sciences

Genetic and electrophysiological studies of Drosophila syntaxin-1A demonstrate its role in nonneuronal secretion and neurotransmission

Article Abstract:

Cloning and characterization of the Drosophila syntaxin-1A gene syx-1A indicate its localization mainly in axons and synapses. An allelic series of loss-of-function mutations lead to embryonic lethality and secretory and morphological defects that are influenced by the severity of the mutant allele. Endogenous synaptic transmission is absent at the neuromuscular junction of partial loss-of-function mutants, and evoked transmission is reduced by 80%. Total lack of syx-1A leads to peripheral and central nervous system morphological abnormalities, damages nonneural secretory events and completely blocks neurotransmitter release, indicating that syntaxin is essential for neurotransmission and that it regulates nonneural secretion.

Author: Bellen, Hugo J., Broadie, Kendal, Perin, Mark S., Schulze, Karen L.
Publisher: Elsevier B.V.
Publication Name: Cell
Subject: Biological sciences
ISSN: 0092-8674
Year: 1995
Secretion, Neural transmission regulation

User Contributions:

Comment about this article or add new information about this topic:

CAPTCHA


Phyllopod functions in the fate determination of a subset of photoreceptors in Drosophila

Article Abstract:

Fate determination of subset of photoreceptors R1, R6, R7 in Drosophila requires the protein encoded by phyllopod (phyl). Genetic data indicate the position of phyl to be downstream of Ras1, raf and yan, and that its functions include the promotion of neuronal differentiation of this subset of receptors. phyl is regulated by Ras1 and is essential for the development of the embryonic nervous system and sensory bristles.

Author: Rubin, Gerald M., Therrien, Marc, Chang, Henry C., Solomon, Noah M., Karim, Felix D., Wolff, Tanya, Wassarman, David A.
Publisher: Elsevier B.V.
Publication Name: Cell
Subject: Biological sciences
ISSN: 0092-8674
Year: 1995
Physiological aspects, Nervous system, Evolution (Biology), Photoreceptors

User Contributions:

Comment about this article or add new information about this topic:

CAPTCHA


Drosophila fragile X-related generegulates the MAP1B homolog Futsch to control synaptic structure and function

Article Abstract:

Results indicate that fragile X-mental retardation gene homolog acts as a translational repressor of the microtubule-associated Futsch gene in the regulation of synaptic microtubule cytoskeleton in Drosophila.

Author: Rubin, Gerald M., Zhang, Yong Q., Bailey, Adina M., Matthies, Heinrich J.G., Renden, Robert B., Smith, Mark A., Speese, Sean D., Broadie, Kendal
Publisher: Elsevier B.V.
Publication Name: Cell
Subject: Biological sciences
ISSN: 0092-8674
Year: 2001
United States, Fragile X syndrome, Structure-activity relationships (Biochemistry), Synaptic transmission

User Contributions:

Comment about this article or add new information about this topic:

CAPTCHA


Subjects list: Analysis, Genetic aspects, Drosophila, Neural transmission
Similar abstracts:
  • Abstracts: Genetic variation of morphological traits in Drosophila melanogaster under poor nutrition: isofemale lines and offspring-parent regression
  • Abstracts: Sprouty, an intracellular inhibitor of Ras signaling. Drosophila rhomboid-1 defines a family of putative intramembrane serine proteases
  • Abstracts: Structural and functional analysis of the mitotic rotamase pin1 suggests substrate recognition is phosphorylation dependent
  • Abstracts: Cdc13 deliveres separate complexes to the telomere for end protection and replication. Switching and signaling at the telomere
  • Abstracts: Control of developmental regulators by Polycomb in human embryonic stem cells. Genome-wide map of nucleosome acetylation and methylation in yeast
This website is not affiliated with document authors or copyright owners. This page is provided for informational purposes only. Unintentional errors are possible.
Some parts © 2025 Advameg, Inc.