PXD061426

PXD061426 is an original dataset announced via ProteomeXchange.

Title	CaMKI dysregulation leads to autism-related phenotypes in precise synaptic connectivity, sleep, social behavior, and aging-dependent degeneration in Drosophila
Description	Postmortem studies reveal increased density of synapses in brains of individuals with autism spectrum disorder (ASD. These observations have led to the hypothesis that defects in synaptic pruning may contribute to ASD pathology. Synaptic pruning, also called synaptic elimination or refinement, is a neuroplastic process involving the removal of ectopic synapses formed in the initial stages of neuronal development. Studies in vertebrates and invertebrates indicate that a crucial factor regulating synaptic pruning is neuronal activity, which was first hypothesized by Nobel laureates Hubel and Wiesel in the 1960s. Studies at the vertebrate retina as well as the mammalian and Drosophila neuromuscular junction (NMJ) indicate that waves of prenatal electrical activity and calcium (Ca2+) oscillations regulate the withdrawal of off-target synaptic contacts. Ca2+ oscillations regulate Ca2+-dependent molecular factors such as kinases (e.g. CaMKII), phosphatases (Calcineurin), and Ca2+-dependent adenylyl cyclases, which in turn regulate intracellular cyclic AMP (cAMP) levels for synaptic pruning in mammalian visual neurons and at the Drosophila NMJ21. Whereas a model to explain the refinement of synaptic connections often involves mechanisms based on Hebbian-like, spike-timing correlation between synaptic partners, where asynchronous inputs are removed, alternative non-Hebbian mechanisms have also been proposed that rely on activity-dependent modulation of chemorepulsion. Although some molecular aspects underlying activity-dependent synaptic refinement have recently been elucidated what molecules link dynamic levels of neuronal activity and the refinement of synaptic contacts during development remain to be elucidated. Consistent with its contributions to advance our understanding of synaptic development, Drosophila melanogaster has emerged as a suitable genetic model system for investigating fundamental mechanisms associated with ASD.
HostingRepository	PRIDE
AnnounceDate	2025-10-06
AnnouncementXML	Submission_2025-10-05_18:36:32.241.xml
DigitalObjectIdentifier
ReviewLevel	Peer-reviewed dataset
DatasetOrigin	Original dataset
RepositorySupport	Unsupported dataset by repository
PrimarySubmitter	Conor Jenkins
SpeciesList	scientific name: Drosophila melanogaster (Fruit fly); NCBI TaxID: NEWT:7227;
ModificationList	phosphorylated residue; monohydroxylated residue; deamidated residue; iodoacetamide derivatized residue
Instrument	Orbitrap Eclipse

Revision	Datetime	Status	ChangeLog Entry
0	2025-03-03 19:57:20	ID requested
⏵ 1	2025-10-05 18:36:33	announced

Gualtieri C, Smith ZM, Cruz A, Khan Z, Jenkins C, Mishra-Gorur K, Vonhoff FJ, . Biology (Basel), 14(9):(2025) [pubmed]

10.3390/biology14091228;

submitter keyword: LC-MSMS, CAMK4, Label Free,Drosophila, autism, neuronal development

Fernando Vonhoff
contact affiliation	University of Maryland Baltimore County Department of Biological Sciences Baltimore, MD
contact email	fvonhoff@umbc.edu
lab head
Conor Jenkins
contact affiliation	US Army DEVCOM CBC
contact email	conor.c.jenkins.civ@army.mil
dataset submitter

Dataset FTP location NOTE: Most web browsers have now discontinued native support for FTP access within the browser window. But you can usually install another FTP app (we recommend FileZilla) and configure your browser to launch the external application when you click on this FTP link. Or otherwise, launch an app that supports FTP (like FileZilla) and use this address: ftp://ftp.pride.ebi.ac.uk/pride/data/archive/2025/10/PXD061426

PRIDE project URI

• PRIDE
  1. PXD061426
     1. Label: PRIDE project
     2. Name: CaMKI dysregulation leads to autism-related phenotypes in precise synaptic connectivity, sleep, social behavior, and aging-dependent degeneration in Drosophila