The phrase "aberrant material" is correct and usable in written English.
It can be used to describe material that deviates from the norm or expected standards, often in scientific or academic contexts.
Example: "The researchers found that the samples contained aberrant material that could skew the results of their experiment."
Alternatives: "anomalous material" or "deviant material".
Activated by environmental factors, such as nutrient depletion, and intracellular stimuli, such as proteotoxic stress, it provides a highly dynamic quality control mechanism to recycle cellular components, eliminate aberrant materials, and, ultimately, maintain cellular homeostasis.
Analysis by agarose gel electrophoresis and HPLC demonstrated that the aberrant plasmid material's overall primary structure, methylation pattern and topological integrity was indistinguishable from that of reference material.
Collectively, these observations indicate that the accumulation of enlarged late endolysosomal structures containing aberrant storage material is due to the loss of AP-5.
Glial phagocytosis of superfluous neurons and damaged or aberrant neuronal material is crucial for normal development and maintenance of the CNS.
Furthermore, the accumulation of aberrant storage material is reminiscent of features described in many lysosomal storage diseases (LSDs) and is indicative of dysfunction along the endosomal/lysosomal pathway.
These multilamellar structures had morphological features of hybrid organelles (derived from the fusion of endosomes and lysosomes), but were filled with aberrant storage material typified by multiple exaggerated whorls, belts of striations, fingerprint bodies and some intraluminal vesicles.
The questions of what the increase in endolysosome frequency means, why aberrant storage material accumulates, how this impacts neuron survival and what this means for the role of AP-5 are complex.
We show that mutations in AP5Z1 impair AP-5 complex formation and result in the accumulation of multilamellar structures containing aberrant storage material, revealing lysosomal dysfunction as the likely pathogenic mechanism.
Using ultrastructural analysis, we show that these patient-derived lines consistently exhibit abundant multilamellar structures that are positive for markers of endolysosomes and are filled with aberrant storage material organized as exaggerated multilamellar whorls, striated belts and 'fingerprint bodies'.
Ultrastructural analysis of patient-derived lines and HeLa cells depleted of AP-5 ζ demonstrate that the loss of AP-5 results in an accumulation of enlarged multilamellar structures that are filled with aberrant storage material.
