| SQSTM1‐polyubiquitin condensates [19] |
K63‐linked polyubiquitin promotes SQSTM1 phase separation; evidence includes cell‐based puncta/condensates, valency dependence, dynamic condensate behavior, and in vitro/biochemical support in the study. |
Supports autophagic cargo segregation and recruitment of autophagy machinery; productive clearance should be interpreted together with cargo turnover/flux assays rather than MAP1LC3 or SQSTM1 colocalization alone. |
Mammalian cells; cell‐based and biochemical/in vitro assays. |
Strong evidence for SQSTM1‐polyubiquitin condensate formation; functional autophagy evidence is context‐dependent. |
Use “phase‐separated SQSTM1 condensates” where LLPS assays are present; avoid equating SQSTM1 puncta alone with degradation. |
| SQSTM1 filaments presenting ubiquitinated cargo [20] |
Reconstitution/biochemical evidence that SQSTM1 forms filamentous assemblies crosslinked by polyubiquitin; provides mechanistic support for higher‐order cargo organization. |
Shows cargo presentation to MAP1LC3‐family proteins and autophagy machinery; primarily supports cargo recognition and presentation rather than proving complete degradation by itself. |
In vitro reconstitution/biochemical systems with supporting cellular relevance. |
Strong mechanistic evidence for scaffold organization; autophagic degradation requires cellular flux/cargo‐turnover validation. |
Best described as reconstituted SQSTM1 filament/condensate organization, not direct endogenous mammalian flux evidence. |
| NBR1/TAX1BP1‐assisted SQSTM1 ubiquitin condensates [78] |
Reconstitution defines how SQSTM1, NBR1, and TAX1BP1 cooperate in ubiquitin condensate formation and initiation‐factor recruitment. |
Connects ubiquitin condensates to autophagy initiation, including receptor/scaffold recruitment; provides mechanistic support for initiation rather than requiring inference from colocalization alone. |
In vitro reconstitution plus mammalian‐cell relevance. |
Strong mechanistic evidence for condensate‐scaffold organization and initiation coupling. |
Distinguish reconstituted initiation mechanisms from endogenous mammalian flux unless directly assayed. |
| TAX1BP1 threshold licensing of aggrephagy [80] |
Analyzes SQSTM1/NBR1 cargo condensates and threshold‐dependent TAX1BP1 recruitment rather than establishing LLPS solely from puncta. |
TAX1BP1 recruitment advances aggrephagy from cargo collection toward sequestration by promoting assembly of TBK1‐, RB1CC1‐, and ATG9‐positive machinery. |
Mammalian‐cell aggrephagy models with mechanistic cell biology. |
Strong evidence for receptor‐threshold licensing and sequestration steps. |
Use “recruitment/transition toward sequestration” unless degradation/flux endpoints are explicitly measured in the specific experiment. |
| RB1CC1 initiation assemblies induced by ER‐surface Ca2+ transients [65] |
Starvation/Torin1/Ca2+ perturbation induces dynamic, fusion‐prone RB1CC1 puncta; evidence includes live‐cell multi‐SIM, fusion/coalescence, FRAP recovery, 1,6‐hexanediol sensitivity, Ca2+ dependence, and endogenous RB1CC1 puncta in some assays. |
RB1CC1 puncta associate with ER and MAP1LC3 structures; EI24/Ca2+ perturbations alter RB1CC1/WIPI2/MAP1LC3 puncta, tandem MAP1LC3 reporter readouts, autophagic‐structure maturation, and TEM‐detected autophagic structures. |
Mammalian COS7 and other cells; tagged RB1CC1 systems, endogenous markers, EI24 KO, Ca2+ pharmacology, TEM. |
Strong evidence for liquid‐like RB1CC1 assemblies under defined conditions; endogenous physiological ULK1‐RB1CC1 LLPS should still be stated cautiously. |
Do not generalize all endogenous ULK1‐RB1CC1 puncta as physiological LLPS; label as “condensate‐like” where criteria are incomplete. |
| TBC1D2B autophagy‐initiation condensates [68] |
Reported phase separation of TBC1D2B upon autophagy induction; association with MAP1LC3/GABARAP via LIR and with ATG12 machinery. |
Supports early phagophore assembly and self‐limiting turnover of TBC1D2B; evidence is strongest for scaffold/initiation function. |
Mammalian autophagy‐induction systems; likely tagged/overexpression plus cellular assays. |
Moderate‐to‐strong evidence for an initiation scaffold; exact physiological/endogenous LLPS strength depends on assay context. |
Avoid presenting as equivalent to endogenous mammalian LLPS unless endogenous and flux data are explicitly shown. |
| NCOA4‐ferritin condensates in macro‐ and microferritinophagy [38] |
NCOA4 homodimerization and binding to FTH1/FTL drive liquid‐like ferritin‐NCOA4 condensates. |
Ferritin‐NCOA4 condensates are routed by macroferritinophagy and microferritinophagy to lysosomal/endolysosomal degradation pathways. |
Mammalian ferritinophagy cell models with mechanistic imaging/cell biology. |
Strong evidence for condensate‐associated ferritin turnover. |
Maintain distinction between NCOA4 condensation and downstream iron‐release/ferroptosis consequences. |
| Iron‐induced NCOA4 condensation and noncanonical ferritin turnover [39] |
Iron loading induces NCOA4 condensation and regulates ferritin fate in an iron‐dependent manner. |
Prolonged iron loading redirects ferritin through a TAX1BP1‐dependent, ATG7‐independent noncanonical pathway. |
Mammalian iron‐homeostasis/ferritinophagy models. |
Strong evidence for iron‐regulated NCOA4 condensation and ferritin routing. |
Specify ATG7‐independent/noncanonical context; do not merge with canonical macroautophagy without qualification. |
| OPTN/CALCOCO2 sheet‐like condensates in Parkin‐mediated mitophagy [74] |
OPTN and CALCOCO2 form sheet‐like, liquid‐like condensates on ubiquitinated mitochondria; dynamic/fluid behavior is examined in live cells. |
Fluidity is functionally linked to ATG9 vesicle recruitment and mitophagy activity; reducing condensate fluidity suppresses mitophagy. |
Mammalian PINK1/PRKN mitophagy models; live‐cell imaging and functional perturbation. |
Strong mammalian evidence for adaptor condensates during mitophagy. |
Present as Parkin‐dependent mitophagy context; do not generalize to all mitophagy modes. |
| TBK1‐phosphorylated OPTN filaments with polyubiquitin and MAP1LC3 [44] |
TBK1‐phosphorylated OPTN forms filamentous condensates with M1‐linked polyubiquitin and co‐condenses with MAP1LC3‐positive membranes; structural/ultrastructural approaches support membrane association. |
Supports cargo sequestration and membrane engagement; strongest for structural coupling rather than complete lysosomal degradation. |
Biochemical/structural and mammalian‐relevant systems; cryo‐ET/ultrastructure noted in manuscript discussion. |
Strong structural/mechanistic evidence for receptor‐condensate membrane coupling. |
Co‐condensation with MAP1LC3 should not be equated with productive autophagic flux unless flux/degradation assays are present. |
| CCT2‐mediated aggrephagy of low‐liquidity/solid aggregates [81] |
CCT2 preferentially associates with low‐liquidity FUS condensates and solid aggregates; in vitro recruitment assays show preference for solid aggregates over liquid granules. |
CCT2 binds aggregation‐prone proteins independently of polyubiquitin and interacts with ATG8‐family proteins through a noncanonical VLIR motif; promotes lysosome‐dependent degradation of solid aggregates and reduces endogenous polyQ‐HTT in mouse striatum. |
Mammalian cells, in vitro aggregate recruitment, yeast conservation for solid Ape1(P22L), and mouse brain/striatum evidence. |
Strong evidence for CCT2 as a solid‐aggregate aggrephagy receptor. |
The original study notes unresolved mechanisms for clearance/fragmentation of large inclusion bodies; avoid implying all solid aggregates are readily cleared. |
| Stress‐granule material‐state transitions and autophagic clearance [45] |
Stress granules show LLPS‐like assembly and can mature toward less dynamic states; material‐state evidence varies by study and stress condition. |
Autophagy contributes to stress‐granule clearance in defined contexts; TRIM21/G3BP1 and SQSTM1/CALCOCO2 pathways modulate clearance. |
Yeast and mammalian stress models; context‐dependent autophagy assays. |
Moderate‐to‐strong evidence for autophagic clearance of stress granules; LLPS evidence depends on specific experimental criteria. |
MAP1LC3/SQSTM1 association with stress granules should be interpreted as recruitment unless flux/cargo turnover is shown. |
| HSPA8 condensates in antibacterial xenophagy [77] |
HSPA8 forms liquid‐like condensates during intracellular bacterial infection and enriches RHOB and BECN1. |
Promotes antibacterial autophagic flux by stabilizing local RHOB‐BECN1 signaling. |
Mammalian infection/xenophagy model. |
Strong functional evidence for condensate‐assisted xenophagy in this model. |
Do not generalize to all xenophagy pathways without additional evidence. |
| SQSTM1 condensates in lysophagy regulated by HSPB1 [56], [57] |
Damaged lysosomes recruit SQSTM1‐positive bodies/condensates; HSPB1 regulates SQSTM1 condensate organization after lysosomal damage. |
Functional lysophagic flux and damaged‐lysosome clearance are supported in the cited studies. |
Mammalian lysosomal‐damage models. |
Strong evidence for receptor‐body organization and lysophagy; LLPS terminology should follow assays used in each study. |
Use “SQSTM1‐positive bodies/condensates” where strict LLPS criteria are incomplete. |
| TFEB nuclear condensates and autophagy‐lysosome transcription [52–54] |
TFEB undergoes phase separation at CLEAR motif‐containing chromatin regions; material properties and surfactant‐like regulators modulate interfacial behavior and transcriptional output. |
Regulates transcription of autophagy–lysosome genes and autophagic/lysosomal capacity; it is not direct cargo degradation. |
Mammalian nuclear/transcriptional systems; perturbation of TFEB condensate material properties. |
Strong evidence for TFEB phase separation and transcriptional regulation of autophagy–lysosome genes. |
Describe as indirect regulation of autophagy capacity, not direct condensate cargo clearance. |
| PolyQ aggregate material state and autophagic accessibility [46] |
Distinguishes non‐fibrillar/amorphous vs. fibrillar polyQ aggregate states by imaging/ultrastructure. |
Autophagy preferentially engages/degrades non‐fibrillar polyQ aggregates, whereas fibrillar structures are less productively captured. |
Mammalian polyQ disease models with ultrastructural analyses. |
Strong evidence that aggregate material state influences autophagic accessibility. |
This supports state‐dependent accessibility, but does not mean all solidified aggregates are invisible to autophagy receptors. |
| Membrane wetting/wrapping of phase‐separated compartments [47, 48] |
Physical modeling and selected experimental systems link surface tension, contact angle, wetting state, and membrane mechanics to condensate–membrane interactions. |
Predicts complete engulfment, partial wrapping, piecemeal degradation, or stalled association; does not itself prove lysosomal degradation without flux/delivery assays. |
Theoretical/physical modeling plus selected experimental observations. |
Useful working model for condensate–membrane coupling. |
Should be presented as a working model, not a universal rule; receptor density, lipid composition, curvature, and lysosomal capacity may modify outcomes. |
| Yeast Atg1/PAS phase separation [5, 105] |
Atg13‐Atg17 multivalent interactions drive phase separation of the Atg1 complex; PAS condensates are dynamic and coalesce on the vacuolar membrane. |
Organizes hierarchical recruitment of downstream Atg proteins and supports autophagosome formation in yeast. |
Yeast and in vitro/reconstitution systems. |
Strong non‐mammalian mechanistic evidence for LLPS‐based initiation‐site organization. |
Valuable for conservation and mechanism, but should not be treated as direct endogenous mammalian evidence. |
| C. elegans PGL granules and autophagic degradation [8] |
mTOR regulates phase separation/material state of PGL granules in C. elegans. |
Material state affects autophagic degradation of PGL granules. |
C. elegans organismal model. |
Strong non‐mammalian evidence for material‐state‐dependent autophagy. |
Use as conserved‐principle evidence, not as direct mammalian autophagy evidence. |
| NUFIP1‐mediated ribophagy [82] |
No strong evidence in the cited work that ribosomes undergo LLPS as cargo; mechanism is receptor‐mediated cargo capture. |
NUFIP1 links ribosomes to MAP1LC3B during starvation‐induced ribophagy. |
Mammalian starvation‐induced ribophagy model. |
Strong receptor‐function evidence; not evidence for cargo LLPS. |
Use as an example of receptor‐mediated spatial organization rather than phase‐separated cargo condensates. |