Blebs by the numbers

Measured sizes, lifetimes and speeds of blebs and the tensions, pressures and cytoplasmic properties behind them, each with system, method and source, and what the numbers mean.

A bleb is a mechanical event: a patch of plasma membrane loses the support of the cortex, the thin layer of actin filaments and myosin motors that lines it, the pressure of the cytoplasm pushes it outward, and a new cortex forms under it and pulls it back. Whether a proposed mechanism can work is therefore a quantitative question. In the spirit of Cell Biology by the Numbers (Milo and Phillips, 2015) and the BioNumbers database (Milo et al., 2010), this page gathers the measured values, each traceable to its source.

Each table row reports one quantity, measured by one method in one system, with the error type and the number of cells or blebs where the source states them, in the original units with conversions in brackets. “Inferred” values were calculated through the model named in the Method column, and “estimated” values come from scaling arguments. In vitro systems and sources we hold only as an abstract are marked, ◆ marks our own work, and “Comparison” rows come from cells in which blebs were not studied or from giant amoebae. The rows should not be averaged: the spread between them shows how much a quantity depends on the cell, its condition and the method.

The page moves from what can be seen (size, duration and speed) to the forces behind it: cortical and membrane tension, attachment, cortex structure, pressure and the material properties of the cytoplasm. The mechanisms are explained in Physics of blebs.

Bleb size

Blebs are small compared with the cells that make them. Most sizes in the table lie between about 1 and 5 µm, from a mean radius of about 1.5 µm on M2 melanoma cells, a human line that lacks the actin cross-linker filamin and blebs continuously, to about 4.6 µm for latrunculin-induced blebs on metaphase HeLa cells (Charras et al., 2008). Confinement can produce much larger blebs: a leader bleb, the single elongated bleb that leads a confined melanoma cell, covered about 13% of the area of the cell body (Logue et al., 2015).

Studies that changed one factor at a time show that size reflects a balance between what drives growth and what resists it. Ablation blebs in L929 fibroblasts were larger the higher the cortical tension (Tinevez et al., 2009). Reducing the function of the ERM proteins that link membrane to cortex enlarged the blebs of zebrafish prechordal plate progenitors from about 16% to about a quarter of the projected cell area (Diz-Muñoz et al., 2010). And knocking down Eps8, which caps and bundles actin, shrank the leader blebs of A375 melanoma cells to about 8% of the cell body and, in rounded cells, lowered cortical tension and pressure (Logue et al., 2015).

How size is reported varies as much as size itself: diameter, radius, height, projected area or volume, in living or fixed cells, so rows can rarely be compared without assuming a shape. Fixed cells need care, since the 0.2–1.5 µm blebs seen by scanning electron microscopy were on dehydrated cells, whose shrinkage the authors mention (Porter et al., 1973). Within one population, final volumes of blebs on M2 and related melanoma cells spanned 5–125 µm³, yet each bleb grew at a constant rate proportional to its final volume, so large blebs filled faster rather than for longer (Cunningham, 1995).

The geometry of the cortex matters too: vesicles with a reconstituted actomyosin cortex formed one large bleb when the network filled the vesicle, but several small ones when it formed a thin membrane-anchored layer (Loiseau et al., 2016). Still missing is a comparison of many cell types measured in the same way, and only two rows come from living embryos, one of them for inverse blebs, which bulge into the cell from the lumen of a growing blood vessel (Diz-Muñoz et al., 2010; Gebala et al., 2016).

Lifetime and phase durations

A bleb on a cultured cell lives for tens of seconds to a few minutes, and its cycle is lopsided. In M2 cells, expansion took 4–7 s, the bleb then stayed still for 10–20 s, and retraction took 40–60 s (Cunningham, 1995). In our reading, the asymmetry reflects the bleb cycle: expansion needs only pressure and a freed membrane, whereas retraction must wait until a new cortex has assembled and become contractile, which took about 30 s in the same cells (Charras et al., 2006).

Other systems lie far from these values. Dictyostelium blebs expanded in about 0.5 s, close to the time resolution of the imaging (Zatulovskiy et al., 2014), and the membrane of Entamoeba histolytica separated from the cortex in less than 0.1 s (Maugis et al., 2010). At the other extreme, inverse blebs in zebrafish blood vessels took up to about 10 min to expand and retract (Gebala et al., 2016), and in chick primordial germ cells leaving blood vessels a single large bleb persisted for 15–30 min at the onset of exit (Morita et al., 2026).

Durations also depend on how each study defined its phases and how often it took images, from 15 frames per second to one every 20 s. Only the three rows from embryos come from cells in tissues.

Expansion and retraction speed

Bleb fronts advance at a few tenths of a micrometer to a few micrometers per second and retract more slowly: on M2 cells, maximal expansion averaged 0.25 µm/s and retraction 0.047 µm/s (Charras et al., 2008). Dictyostelium blebs expanded at about 1.8 µm/s (Zatulovskiy et al., 2014), and the Entamoeba front moved at 10–20 µm/s during its first few hundred milliseconds (Maugis et al., 2010). In circus movement, where a bleb travels around a rounded cell, the front advanced at about 1.6 µm/s on Xenopus blastomeres while the rear retracted at about 0.4 µm/s (Charras et al., 2008).

These speeds have carried mechanistic arguments. Keller and Bebie (1996) found that the membrane of Walker carcinosarcoma cells advanced at 1.2–4.1 µm/s, faster than the actin elongation rates then known, and concluded that their data fitted best with protrusion driven by hydrostatic pressure. Charras et al. (2008) turned the argument around, using the maximal expansion speed, with an assumed pressure and viscosity, to estimate the pore size of the cytoplasmic mesh (see the last section).

Speeds are given as maximal, mean or initial values, for a front or for a volume, and a volume rate such as the 30 µm³/s of some M2 blebs (Cunningham, 1995) cannot be turned into a front speed without knowing the bleb’s shape. Only three rows give retraction speeds, too few to say how retraction depends on the cell.

Cortical tension

Cortical tension, the in-plane tension that myosin motors generate in the cortex, is what pressurizes the cell. Measured on whole cells, it varies about tenfold, from about 170 pN/µm in suspended HeLa cells (Chugh et al., 2017) to about 1,600 pN/µm in Dictyostelium and in rounded A375 melanoma cells (Gerald et al., 1998; Logue et al., 2015).

By Laplace’s law, the excess pressure in a spherical cell equals twice the tension divided by the radius. For suspended L929 fibroblasts, 8.5 µm in radius with a tension of about 410 pN/µm, this gives the excess pressure of about 100 Pa that Tinevez et al. (2009) state, within an order of magnitude of most pressures measured with probes (see the last section).

Tension matters for blebbing above all through a threshold. In L929 cells whose tension was lowered with an inhibitor of Rho-associated kinase (ROCK), no bleb grew after laser ablation of the cortex below about 200 pN/µm (Tinevez et al., 2009), and no threshold has been located in other cells. Lower tension does not always mean fewer blebs, however: Dictyostelium cells lacking the GTPase racE had about a fifth of the wild-type tension, yet most made violent shape changes when dividing in suspension, some with large blebs, which the authors attributed to a weakened cortex (Gerald et al., 1998).

Aspiration and compression with a flat cantilever in an atomic force microscope (AFM) measure the tension of the whole surface of rounded cells, cortex and membrane together. Values inferred from bleb size inherit the uncertainty of an assumed elastic modulus, hence the 130–900 pN/µm estimate for HeLa cells (Charras et al., 2008). The tension of a cell migrating with blebs has not been measured.

Membrane tension and membrane–cortex attachment

The plasma membrane on its own carries much less tension than the cortex. On blebs, which lack a cortex, it was about 1 pN/µm from fluctuations of the bleb outline and 11–12 pN/µm from tethers, thin membrane tubes pulled from the surface (Dai and Sheetz, 1999; Charras et al., 2008), far below whole-cell cortical tensions. In our reading, this difference is the mechanical basis of a bleb: once freed from the cortex, the membrane resists the pressure with little more than its own small tension.

Tethers pulled from cortex-backed membrane give higher, apparent membrane tensions, about 30–46 pN/µm, because the membrane must also be torn from the cortex (Dai and Sheetz, 1999; Diz-Muñoz et al., 2010). Comparing them with tethers from blebs separates the two: attachment accounted for about 11 pN of tether force in M2 cells (Dai and Sheetz, 1999), whereas in fish keratocytes the two forces did not differ significantly (Lieber et al., 2013). Method matters as much as cell type: on M2 blebs, values ranged from 0.81 pN/µm by fluctuation analysis to an effective 71 pN/µm by interferometry late in growth, which includes any new cortex (Charras et al., 2008; Peukes and Betz, 2014).

Blebs have also served as cortex-free membrane in studies of how tension spreads. Within a bleb, a pull on one tether reached another in less than 1 s in HeLa cells and in less than 0.1 s in neutrophil-like HL-60 cells (Shi et al., 2018; De Belly et al., 2023), whereas on intact cells neither study saw nearby tethers coupled. In HL-60 cells, however, a light-induced protrusion raised the tension at two distant tethers within about a second (De Belly et al., 2023). In HeLa cells migrating under confinement with a leader bleb, a membrane-tension probe showed no gradient over 10–30 µm (García-Arcos et al., 2025 ◆).

How firmly the membrane is held to the cortex is the least settled quantity on this page. The energies in the next table span three orders of magnitude, from about 10⁻⁶ J/m², estimated from the angle at which tearing M2 blebs left the cortex (Charras et al., 2008), to about 10⁻³ J/m² from the suction needed to detach the membrane in Dictyostelium, a value we hold only from the abstract (Merkel et al., 2000). Each study defines attachment differently and infers the energy through a model, and in our reading the aspiration value may also include breaking the cortex itself.

The clearest link between attachment and blebbing comes from the one study that measured both: lowering ERM function in zebrafish progenitors cut the adhesion energy three- to fourfold, without changing cortical tension, and enlarged blebs in isolated cells and in the embryo (Diz-Muñoz et al., 2010). A related number is the suction that starts blebbing, about 170 Pa through a micropipette in Walker carcinosarcoma cells (Rentsch and Keller, 2000), the same order as the pressures measured inside cells.

Cortex thickness, assembly and turnover

The cortex is thin compared with a bleb, but how thin depends on the method: electron microscopy of fixed blebs gave 10–50 nm (Charras et al., 2006; Charras et al., 2008), whereas optical and magnetic methods mostly gave 116–253 nm (Clark et al., 2013; Laplaud et al., 2021; Cassani et al., 2024 preprint). In our reading, method and preparation explain part of this gap (proposed). Within one method the comparison is cleaner. By dSTORM super-resolution imaging, the reassembled cortex of isolated HeLa blebs was 116 nm thick, against 143 nm in rounded cells (Cassani et al., 2024 preprint), and in one ablation bleb followed live the cortex thickened from about 50 to about 200 nm as the bleb retracted (Clark et al., 2013).

The new cortex assembles within the lifetime of a bleb. In M2 cells, ezrin appeared at the bleb membrane about 5 s before actin and myosin about 7 s after it, and a contractile cortex was complete in about 30 s (Charras et al., 2006). The cortex also turns over quickly, actin in retracting blebs recovering from photobleaching about four times faster than in the mature cortex (Fritzsche et al., 2013), so in our reading the cortex that pulls a bleb back is renewed while it contracts. All rows in this section come from cultured cells, none from a cell migrating with blebs.

Intracellular pressure and the cytoplasm

Intracellular pressure, the excess of cytoplasmic over external pressure, is what inflates a bleb. Probes inserted into the cytoplasm read about 400 Pa in blebbing M2 cells, the pressure at the bottom of a water column about 4 cm high (our conversion), and 400–600 Pa in HeLa cells (Malboubi et al., 2026). With a ROCK inhibitor, which stops blebbing, the pressure of M2 cells fell to about 100 Pa, and the authors concluded that blebs cease to form below about this value. Non-blebbing fibroblasts measured with the same kind of probe span a range that includes these values, from about 300 Pa in cells with lamellipodia to about 2,200 Pa in cells forming lobopodia, blunt protrusions distinct from blebs (Petrie et al., 2014). In our reading, blebbing cells do not stand out by an unusually high pressure.

Pressures inferred from the blebs themselves, through an assumed elastic modulus or a tether tension, are lower: 17–110 Pa in M2 cells and 45–300 Pa in metaphase HeLa cells (Dai and Sheetz, 1999; Charras et al., 2008). Each estimate inherits the uncertainty of its assumption, and blebs have not been calibrated as pressure gauges against a probe in the same cells. The 1–10 Pa estimated for Entamoeba is a different quantity, the pressure difference across the cortex that drives the bleb front (Maugis et al., 2010).

The oldest pressure numbers, from pseudopods of giant amoebae rather than from blebs, fall in the same range of hundreds of pascals. About 110 Pa applied to a pseudopod of Chaos chaos sealed in a capillary stopped its streaming (Allen and Roslansky, 1959), and a probe in Amoeba proteus read a pressure that rose from about 0.3 to 1.4 kPa before a pseudopod formed (Yanai et al., 1996).

A single pressure per cell may itself be a simplification. In fibroblasts moving through a three-dimensional matrix, pressure was about 2,400 Pa in front of the nucleus and about 900 Pa behind it (Petrie et al., 2014), and M2 cells kept blebbing beside a pipette that released pressure locally, which the authors read as pressure held in compartments (Malboubi et al., 2026). Whether pressure evens out across a blebbing cell faster than a bleb grows is an open question (Physics of blebs).

How fast a pressure change spreads depends on the cytoplasm, which in two independent tests behaved as a poroelastic material, an elastic mesh soaked in fluid (Charras et al., 2009; Moeendarbary et al., 2013). Its diffusion constants, about 5 µm²/s from local osmotic perfusion and 40–61 µm²/s from AFM indentation, give an evening-out time over 10 µm of about 20 s and 2.5 s (our arithmetic), comparable to the seconds a bleb takes to grow; the two methods also act over different times, tens of seconds and under a second. In M2 cells, two independent estimates point to pores of the order of 10 nm (Charras et al., 2008).

No viscosity in the table comes from a blebbing cell. The only values, from giant amoebae, differ by up to two orders of magnitude with the method, from about 4.5 mPa·s by particle tracking over milliseconds (Rogers et al., 2008) to 0.01–0.9 Pa·s from magnetic pulling and streaming profiles (Allen and Roslansky, 1959; Yagi, 1961). In our reading, the methods probe the cytoplasm over very different times and distances, from the fluid between filaments to whole streams.

Where to read more

The experiments behind many rows are described in more detail on the pages below.

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