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Newly discovered protein controls the space between mitochondrial membranes (opens in a new tab)

news-medical.net · 2026-10-23

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The story

Newly discovered protein controls the space between mitochondrial membranes

news-medical.net · 2026-10-23

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Mostly supported

Every claim we could check holds up. Five of six claims match the study. This overall rating is based only on the claims we could check. One claim the study doesn't address.

5 supported
1 not covered

Open claim evidence

The source study

SPRIZ (CCDC127) protein conserved in deuterostome animals is a rigid OMM-IMM tether that locally sets mitochondrial IMS volume.

Science Advances · 2026

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6 claims in this story

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Claim 1 of 6Not coveredThe story says the same molecular pillar architecture was found in humans and every other vertebrate species examined, and that evolutionary analysis places SPRIZ's emergence around 500 million years ago near the origin of vertebrates.View evidenceHide evidence

As statedroughly 500 million years

Why this verdict

The abstract-level profile supports conservation/vertebrate-specific structural features in general, but it does not provide enough detail to verify the story’s more specific claims that the same pillar architecture was found in humans and every other vertebrate species examined or that evolutionary analysis dates SPRIZ emergence to roughly 500 million years ago near vertebrate origins.

Study evidence

Cryo-electron tomography of native mitochondria revealed rod-like densities spanning the intermembrane space (IMS).

“Cryo-electron tomography of native mitochondria revealed rod-like densities spanning the intermembrane space (IMS), consistent with SPRIZ's predicted rigid coiled-coil architecture and membrane-spanning topology.”

Claim 2 of 6SupportedA new study led by a University of Ottawa Faculty of Medicine investigator reports that the volume of the mitochondrial intermembrane space is genetically controlled and adjustable.View evidenceHide evidence

As statedthe volume of the IMS is genetically controlled and adjustable

Why this verdict

The abstract-level profile supports the paper’s framing that SPRIZ/CCDC127 is a genetically encoded mitochondrial tether that sets local OMM–IMM separation and that experimental SPRIZ/MARTINI manipulations and knockout alter IMS geometry. The story’s wording is broad, but it is framed as what the study reports and is consistent with the abstract-level conclusions, with the caveat that much of the quantified evidence is in mouse liver/ex vivo mitochondria.

Study evidence

Cryo-electron tomography of native mitochondria revealed rod-like densities spanning the intermembrane space (IMS).

“Cryo-electron tomography of native mitochondria revealed rod-like densities spanning the intermembrane space (IMS), consistent with SPRIZ's predicted rigid coiled-coil architecture and membrane-spanning topology.”

Study evidence

SPRIZ expression is associated with ~3-fold expansion of IMS area in mouse liver mitochondria measured by 2D EM morphometry.~3-fold

“In mouse liver, two-dimensional morphometry measured ∼3-fold expansion of IMS area with SPRIZ and ∼5.5-fold with lengthened mitochondrial artificial increaser of the IMS (MARTINI)”

Claim 3 of 6SupportedPublished in Science Advances, the study identifies SPRIZ as a key protein that cells use to shape mitochondrial internal architecture.View evidenceHide evidence

Why this verdict

The paper profile identifies SPRIZ/CCDC127 as a conserved rigid OMM–IMM tether that physically spans the IMS and sets local membrane separation, making the story’s description of SPRIZ as a key protein shaping mitochondrial internal architecture supported at abstract depth.

Study evidence

Cryo-electron tomography of native mitochondria revealed rod-like densities spanning the intermembrane space (IMS).

“Cryo-electron tomography of native mitochondria revealed rod-like densities spanning the intermembrane space (IMS), consistent with SPRIZ's predicted rigid coiled-coil architecture and membrane-spanning topology.”

Study evidence

SPRIZ expression is associated with ~3-fold expansion of IMS area in mouse liver mitochondria measured by 2D EM morphometry.~3-fold

“In mouse liver, two-dimensional morphometry measured ∼3-fold expansion of IMS area with SPRIZ and ∼5.5-fold with lengthened mitochondrial artificial increaser of the IMS (MARTINI)”

Claim 4 of 6SupportedThe team reports that SPRIZ bridges the two mitochondrial membranes and acts like a molecular pillar that holds the intermembrane space open.View evidenceHide evidence

Why this verdict

The profile reports cryo-ET rod-like densities spanning the IMS and interprets SPRIZ as an ~18-nm homodimeric tether anchored in the OMM and inserted into the IMM. That supports the story’s molecular-pillar/bridging description, though the abstract-level profile notes that direct molecular identification of the densities is inferential rather than fully detailed.

Study evidence

Cryo-electron tomography of native mitochondria revealed rod-like densities spanning the intermembrane space (IMS).

“Cryo-electron tomography of native mitochondria revealed rod-like densities spanning the intermembrane space (IMS), consistent with SPRIZ's predicted rigid coiled-coil architecture and membrane-spanning topology.”

Claim 5 of 6SupportedIn laboratory experiments, altering SPRIZ substantially changed the size of the intermembrane space, and expanding it changed molecular access and mitochondrial calcium uptake.View evidenceHide evidence

As statedsubstantially changed the size of the IMS

Why this verdict

The abstract-level profile reports experimental SPRIZ-associated and engineered-tether-associated IMS expansion, including ~3-fold and ~5.5-fold 2D morphometry changes, 3D tomography confirmation for MARTINI, increased 14C-mannitol IMS accessibility, and impaired mitochondrial Ca2+ uptake. The causal laboratory framing is supported by the experimental manipulations, although assay details, sample sizes, and exact Ca2+ effect magnitude are not available at abstract depth.

Study evidence

SPRIZ expression is associated with ~3-fold expansion of IMS area in mouse liver mitochondria measured by 2D EM morphometry.~3-fold

“In mouse liver, two-dimensional morphometry measured ∼3-fold expansion of IMS area with SPRIZ and ∼5.5-fold with lengthened mitochondrial artificial increaser of the IMS (MARTINI)”

Study evidence

3D electron tomography of mouse liver mitochondria confirmed that the engineered lengthened tether (MARTINI) produced greater OMM–IMM separation and a change described as 'normalized IMS volume.'

“3D electron tomography confirmed MARTINI's greater OMM-IMM separation and normalized IMS volume.”

Claim 6 of 6SupportedExperiments in mice found that removing the gene altered mitochondrial membrane spacing while leaving overall mitochondrial structure intact and the mice viable.View evidenceHide evidence

Why this verdict

The profile directly states that constitutive Ccdc127/SPRIZ knockout produced viable mice and that liver mitochondria preserved overall ultrastructure while showing modest IMS expansion. This matches the story’s claim, with the qualification that the abstract-level evidence specifies liver mitochondria and a modest spacing change.

Study evidence

Constitutive Ccdc127/SPRIZ knockout produced viable mice.

“Constitutive Ccdc127/SPRIZ knockout produced viable mice and, in liver mitochondria, preserved overall ultrastructure but caused modest IMS expansion”

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Context layer

What the story left out

Important study details the story did not include.

3D electron tomography confirms that MARTINI increases OMM–IMM separation and changes/normalizes IMS volume.
The story generally says laboratory expansion changed IMS size, but the supplied presentation does not mention the MARTINI-specific 3D tomography validation or the abstract’s more precise phrasing about normalized IMS volume.
From 3D electron tomography with reconstruction/segmentation
Important knockout-model limitation: the knockout result is reported for liver mitochondria, and constitutive knockout could involve developmental compensation or miss tissue-specific phenotypes.
The story notes mouse viability and preserved overall structure, but the supplied caveats do not include the paper profile’s liver-specific scope or compensation/tissue-specificity limitations.
From Constitutive Ccdc127/SPRIZ knockout mouse with ex vivo liver mitochondrial ultrastructural analysis

7 things the story did carry across

SPRIZ/CCDC127 is identified and structurally characterized as a conserved rigid tether spanning the mitochondrial intermembrane space and setting local OMM–IMM separation.
Cryo-electron tomography evidence for IMS-spanning rod-like densities is interpreted as consistent with SPRIZ’s predicted tether architecture.
SPRIZ expression and the engineered lengthened tether MARTINI alter IMS geometry in mouse liver mitochondria, with reported ~3-fold and ~5.5-fold 2D IMS area expansions.
Expanded IMS volume is functionally validated by increased 14C-mannitol accessibility to the IMS.
Expanded IMS volume is associated with impaired mitochondrial Ca2+ uptake in ex vivo mitochondrial assays.
Constitutive Ccdc127/SPRIZ knockout mice are viable and show preserved overall liver mitochondrial ultrastructure with modest IMS expansion.
Evolutionary/conservation context is present only at a high level in the abstract-depth profile, not with the story’s human/all-vertebrate/500-million-year specificity.

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study summary

Lead result

ex vivo animal

1Lead resultex vivo animalIdentify and structurally characterize SPRIZ/CCDC127 as a conserved rigid OMM–IMM tether that physically spans the mitochondrial intermembrane space and sets local OMM–IMM separation (IMS volume).Expand

In plain English

Cryo-electron tomography of isolated native mitochondria revealed rod-like densities spanning the mitochondrial intermembrane space (IMS). These densities are interpreted as being consistent with the predicted ∼18-nanometer rigid coiled-coil homodimer of SPRIZ (CCDC127), anchored in the outer mitochondrial membrane (OMM) and inserting into the inner mitochondrial membrane (IMM) via vertebrate-specific hydrophobic loops, supporting the model that SPRIZ physically tethers and sets local OMM–IMM separation.

Key findings

Cryo-electron tomography of native mitochondria revealed rod-like densities spanning the intermembrane space (IMS).
Observed IMS-spanning rod-like densities are interpreted as consistent with a predicted ∼18-nanometer rigid coiled-coil SPRIZ homodimer anchored in the OMM and inserting into the IMM, supporting a tethering topology that would set local OMM–IMM separation.

“Cryo-electron tomography of native mitochondria revealed rod-like densities spanning the intermembrane space (IMS), consistent with SPRIZ's predicted rigid coiled-coil architecture and membrane-spanning topology.”

What this piece can’t prove

Cryo-ET provides morphological consistency but not definitive molecular identification; interpretation depends on matching predicted SPRIZ features to observed densities.

2 further details could not be confirmed from the summary.

2ex vivo animalQuantify how SPRIZ and an engineered lengthened tether (MARTINI) alter IMS geometry/volume in mouse liver mitochondria using EM morphometry and tomography.2D EM morphometryExpand

In plain English

In mouse liver mitochondria, 2D electron-microscopy morphometry showed that expression of SPRIZ increases IMS area ~3-fold, while an engineered lengthened tether (MARTINI) increases IMS area ~5.5-fold, indicating tether length alters local OMM–IMM spacing as measured in 2D images.

Key findings

SPRIZ expression is associated with ~3-fold expansion of IMS area in mouse liver mitochondria measured by 2D EM morphometry.~3-fold
An engineered lengthened tether (MARTINI) is associated with ~5.5-fold expansion of IMS area in mouse liver mitochondria measured by 2D EM morphometry.~5.5-fold

“In mouse liver, two-dimensional morphometry measured ∼3-fold expansion of IMS area with SPRIZ and ∼5.5-fold with lengthened mitochondrial artificial increaser of the IMS (MARTINI)”

What this piece can’t prove

2D EM morphometry reports cross-sectional IMS area and does not directly measure 3D IMS volume.
Abstract does not provide experimental details needed to assess potential sampling bias, image selection, or statistical robustness (e.g., n, replicates, error estimates).

1 further detail could not be confirmed from the summary.

3ex vivo animalQuantify how SPRIZ and an engineered lengthened tether (MARTINI) alter IMS geometry/volume in mouse liver mitochondria using EM morphometry and tomography.3D electron tomography with reconstruction/segmentationExpand

In plain English

3D electron tomography and 3D segmentation/quantification in mouse liver mitochondria confirmed that an engineered lengthened tether (MARTINI) produces greater outer-membrane to inner-membrane (OMM–IMM) separation and alters/normalizes intermembrane space (IMS) volume.

Key findings

3D electron tomography of mouse liver mitochondria confirmed that the engineered lengthened tether (MARTINI) produced greater OMM–IMM separation and a change described as 'normalized IMS volume.'

“3D electron tomography confirmed MARTINI's greater OMM-IMM separation and normalized IMS volume.”

What this piece can’t prove

3 further details could not be confirmed from the summary.

4ex vivo animalFunctionally validate that expanding IMS volume changes IMS accessibility and mitochondrial physiology (e.g., Ca2+ uptake).Ex vivo radiotracer mitochondrial accessibility assay (14C-mannitol)Expand

In plain English

Radiotracer 14C-mannitol accessibility assays on mitochondria showed increased accessibility of 14C-mannitol to the intermembrane space (IMS) when IMS volume was expanded (reported alongside SPRIZ/MARTINI manipulations), providing functional validation that morphological IMS expansion increases accessible IMS space.

Key findings

Increased 14C-mannitol accessibility to the mitochondrial IMS was observed when IMS volume was expanded (reported in conjunction with SPRIZ and lengthened-MARTINI manipulations).

“This expansion was functionally validated by increased 14C-mannitol accessibility to the IMS”

What this piece can’t prove

3 further details could not be confirmed from the summary.

5ex vivo animalFunctionally validate that expanding IMS volume changes IMS accessibility and mitochondrial physiology (e.g., Ca2+ uptake).mitochondrial Ca2+ uptake assay (ex vivo)Expand

In plain English

The paper reports that experimental expansion of the mitochondrial intermembrane space (IMS) increased 14C-mannitol accessibility to the IMS and was associated with impaired mitochondrial Ca2+ uptake measured in ex vivo mouse liver mitochondria.

Key findings

Expansion of mitochondrial IMS is associated with impaired mitochondrial Ca2+ uptake.

“and by impaired mitochondrial Ca2+ uptake.”

What this piece can’t prove

3 further details could not be confirmed from the summary.

6in vivo animalDetermine organismal and mitochondrial consequences of constitutive Ccdc127/SPRIZ knockout in mice, including effects on mitochondrial ultrastructure and IMS dimensions.Constitutive Ccdc127/SPRIZ knockout mouse with ex vivo liver mitochondrial ultrastructural analysisExpand

In plain English

Constitutive Ccdc127/SPRIZ knockout mice are viable. Examination of liver mitochondria revealed largely preserved overall ultrastructure but a modest expansion of the intermembrane space (IMS), interpreted as consistent with loss of local outer–inner mitochondrial membrane (OMM–IMM) constraints normally imposed by SPRIZ.

Key findings

Constitutive Ccdc127/SPRIZ knockout produced viable mice.
In liver mitochondria from knockout mice, overall ultrastructure was preserved but the intermembrane space showed a modest expansion, consistent with loss of local OMM–IMM constraints.

“Constitutive Ccdc127/SPRIZ knockout produced viable mice and, in liver mitochondria, preserved overall ultrastructure but caused modest IMS expansion”

What this piece can’t prove

Constitutive knockout design can permit compensatory adaptations that may mitigate phenotypes and confound attribution of direct effects.
Functional consequences of the modest IMS expansion in KO mitochondria are not detailed here.

2 further details could not be confirmed from the summary.

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Method layer