Evidence map›Paper›PMID 40975051›Full record

ArticleCurrent biology : CB2025

Mitochondria transported by Kinesin-3 prevent localized calcium spiking to inhibit caspase-dependent specialized cell death.

Rashna Sharmin, Aladin Elkhalil, Sara Pena, Pranya Gaddipati, Ginger Clark, Pavak K Shah, Mark W Pellegrino, Shai Shaham, Piya Ghose

Abstract read
In one paragraph

Article in Current biology : CB, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

4 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Kinesins inOpen biology · 2025
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

Rashna SharminThe University of Texas at Arlington, Department of Biology, 501 S. Nedderman Dr., Arlington, TX 760109, USA.
Aladin ElkhalilThe University of Texas at Arlington, Department of Biology, 501 S. Nedderman Dr., Arlington, TX 760109, USA.
Sara PenaThe Rockefeller University, Laboratory of Developmental Genetics, 1230 York Ave., New York, NY 10065, USA.
Pranya GaddipatiThe University of Texas at Arlington, Department of Biology, 501 S. Nedderman Dr., Arlington, TX 760109, USA.
Ginger ClarkThe University of Texas at Arlington, Department of Biology, 501 S. Nedderman Dr., Arlington, TX 760109, USA.
Pavak K ShahThe University of California, Los Angeles, Department of Molecular, Cell and Developmental Biology, 610 Charles E Young Dr., Los Angeles, CA 90095, USA.
Mark W PellegrinoThe University of Texas at Arlington, Department of Biology, 501 S. Nedderman Dr., Arlington, TX 760109, USA.
Shai ShahamThe Rockefeller University, Laboratory of Developmental Genetics, 1230 York Ave., New York, NY 10065, USA.
Piya GhoseThe University of Texas at Arlington, Department of Biology, 501 S. Nedderman Dr., Arlington, TX 760109, USA. Electronic address: piya.ghose@uta.edu.

Funding

Glial Control of Neuron Development and Function - Administrative SupplementR35NS105094 · NINDS · ROCKEFELLER UNIVERSITY · PI SHAHAM, SHAI · 2018 to 2025
$8.9M
Enhancing and expanding the CGC Strain CollectionP40OD010440 · OD · UNIVERSITY OF MINNESOTA · PI Aric L Daul, Ann E. Rougvie · 2012 to 2026
$7.5M
Mechanisms of host protection during infection via the mitochondrial unfolded protein responseR35GM128885 · NIGMS · UNIVERSITY OF TEXAS ARLINGTON · PI Mark Watson Pellegrino · 2018 to 2026
$3.0M
In Vivo Genetic Analysis of Compartmentalized Cell EliminationR35GM142489 · NIGMS · UNIVERSITY OF TEXAS ARLINGTON · PI GHOSE, PIYA · 2021 to 2025
$2.3M
Linker cell death regulation in C. elegansR01HD103610 · NICHD · ROCKEFELLER UNIVERSITY · PI SHAHAM, SHAI · 2021 to 2025
$1.8M
Lineage-Specific Mechanisms of Cell Cycle Timing ControlR35GM151199 · NIGMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Pavak Kirit Shah · 2023 to 2026
$1.5M
NICHD NIH HHS R01 HD103610NIGMS NIH HHS R35 GM128885NIGMS NIH HHS R35 GM142489NIGMS NIH HHS R35 GM151199NIH HHS P40 OD010440NINDS NIH HHS R35 NS105094
6 · The paper itself

Abstract

Polarized cells (such as neurons) have distinct compartments with differing functions, subcellular architecture, and microenvironments. Like many cell types, they are subject to programmed elimination as a part of normal development and homeostasis. We investigated the mechanism of specialized cell elimination by studying the embryonic cell death program, compartmentalized cell elimination (CCE), in the scaffolding tail-spike epithelial cell (TSC) of C. elegans. CCE, also seen in Cephalic male (CEM) sensory neurons, is stereotyped and ordered, with distinct programs eliminating each cell compartment-the soma and two segments of the single process, the latter resembling neurite pruning. Here, we report the atypical, compartment-specific roles of two kinesins in mitochondrial transport to regulate CCE. We show that UNC-116/Kinesin-1 is required to transport mitochondria out of the TSC process and that its absence results in distal mitochondrial retention and process persistence. We describe UNC-104/Kinesin-3 in the non-canonical role of mitochondrial transport that is negatively regulated by CED-3/caspase. We identify a degenerative hub of the TSC at the junction of the cell soma and process, characterized by local CED-3/caspase activity, Ca

Indexed as

Caenorhabditis elegansCaenorhabditis elegans ProteinsCalcium SignalingCaspasesKinesinsMitochondriaAnimalsCalciumCell DeathSensory Receptor CellsCaenorhabditis elegans ProteinsCalciumCaspasesced-3 protein, C elegansKinesins

Identifiers

PMID40975051
PMCPMC12462904

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.