Avocado Skin Topography

Laurie Meadows
29 August 2019

Some avocado fruit, such as Mexicola, Topa Topa, and Rincon, have smooth skin. The odd one, such as Lula, has ‘almost’ smooth skin. Most other have skin with varying degrees of ‘roughness’.

Botanically, the bumps on avocado skin are tubercles, as are the bumps on the skin of other fruit, such as lychee and gourds. Avocado tubercles are usually described by terms such as warty, rough, bumpy, or pebbled (further qualified by words such as low, high, slightly, somewhat, moderately, highly, very). The diverse terms used to describe avocado skin surface topography struggle to include two major components – the number of tubercles per unit area of skin (tubercle density) and height/width (‘prominence’). Minor components of skin topography include coalescing of tubercles into ridges; apparently non-tuberculate sharply defined creases; and disorganized reticulation.

The question are: what are tubercles? Why do they exist? How do they arise? This article draws together investigations in other fruit (mainly) which provide, to a degree, plausible initial explanations.

The article was prompted by this Twitter post by Sonia Rios, Subtropical Horticulture Farm Advisor, University of California, showing a ‘sectorial chimera’ in a Hass avocado fruit. A mutation at a very early stage of fruit development causes a zone or sector of ‘smooth’ skin within the otherwise normal ‘rough’ Hass skin.


smooth skin section on the left side of a normal ‘bumpy’ Hass fruit.

As most mutations are ‘loss of function’, blocking or diluting the ‘proper’ operation of a gene, it is fair to suppose this mutated area of skin is due to the direct or indirect blocking of some signal to the skin that ordinarily results in the warty tubercles. Mutations usually happen in the cells of the actively dividing meristem tissues. The various causes of mutations causing chimeras and bud sports are extensively listed in Foster and Aranzana (2018) .

Chimeras in the avocado Skin

According to Foster and Aranzana (2018), angiosperms meristems consist of (generally) 2 outer layers of cells, the tunica, draped over an inner layer, the corpus. The first, outer, layer of the tunica gives rise to the epidermis. The second layer gives rise to sub-epidermal tissues.

Foster and Aranzana (2018) propose color mutations in one sector of a flower are due to a mutation in gene expression in a mericlinal (pole to pole) sectorial chimera affecting either one or both of the tunicate layers. This is illustrated by the pink petal in the advanced flower bud of a white azalea cultivar which serendipitously appeared when I was writing this article. Both the solid color flower (on the left) and the petal mutant are probable L1 mutants ( Foster and Aranzana, 2018).

Mericlinal sectorial chimara in a white azalea.

This principle may also apply a gene (or genes) responsible for the smooth skin sectorial mericlinal chimera in the above photo. This might imply that ‘pebbled’, ‘bumpy’, ‘warty’ or ‘rough’ skin topography in Hass and other avocados with various degrees of tubercule expression is controlled by a single gene, perhaps additively expressed in the outer tunica.

But, anatomically, what is a tubercle anyway, and how does it arise? This is a suprisingly complex question to find a plausible answer to.

Does stomata patterning cause or coincide with tubercle formation?

According to Schroeder (1950), in avocado, the epidermis is made up of a single layer of cells. A second layer, the hypodermis, either one or two cells thick, is usually present immediately under the epidermis. These cells have a natural polymer, cutin, laid down in the cell walls. Under that are parenchyma cells. Stomata are formed by a pair of crescent-shaped epidermal cells (the guard cells) flanking an open pore in the epidermis.

In avocado, stomata have immediately underneath them a mass of loosely packed cells with abundant intercellular spaces. This is believed to make gas exchange maximally efficient.

Schroeder notes that in round relatively smooth skinned avocados the uniform expansion of the skin surface of the growing fruit results in relatively evenly spaced stomata. But in rough skinned genotypes the stomata are “restricted to the elevated mounds of tissues…varieties such as Hass and Dickinson have stomata concentrated in groups on the elevated surfaces of the rind”.

Curiously, Everett et al (2001) – contra Schroeder – found in ‘firm’ green avocados that lenticels (identifiable “as small yellow dots”) “form all over the fruit surface, not just on the lumps.” I examined new season spring-set Hass, Fuerte, 3 seedlings of unknown parentage and a ‘smooth’ skin cultivar in late autumn and found stomata (yellow or cream dots) co-incide to the highest degree with elevated skin relief. If we use a ‘mountain and valley’ analogy, stomata (presumably aka lenticels) are almost entirely confined to mountain slopes and are relatively rare on valley floors.

stomata grouped on Hass tubercles

But in immature fruit there is almost no ‘valley floor space’ and the toe of one ‘mountain’ abuts the toe of adjacent ‘mountains’. This changes as the fruit increases in size. The valley floors that ’emerge’ are easier to observe. (This is best seen in natural light where the shadows cast by surface relief across the fruit surface make topography easy to observe.)

Late-hung last season Hass fruit observed at this stage have lower relief, that is, ‘flattened’ mountains and wider valley. Creasing, unrelated to stomata patterning, becomes either more developed, or more apparent.

The case for tubercle formation being related to tissues associated with stomata looks promising. So what is the importance of clustered stomata?

In leaves, Dow et al (2014) define the “proper spacing” of stomata (on Arabidopsis leaves) as less than 5% of stomata in clusters. This spacing (scaling with increasing stomata number) achieves maximum water vapor conductance, maximum gas exchange and consequent net carbon assimilation, as well as maximal stomatal responsiveness to increases in CO2 concentration.

In contrast, the authors found that genotypes with greater than 19% of stomata in clusters had (> 19% clustering) did not. Genotypes with clustering also had reduced net carbon assimilation and “impaired” stomatal response to increasing CO2 concentrations, and impaired stomatal responses. Water use efficiency was largely unaffected by clustering.

A mutation in a gene or genes controlling the stomatal patterning process could cause clustering.The clustering phenomenon occurs when the protodermal cells in the epidermis which produce stomatal guard cells fail to divide asymmetrically. Asymmetrical division creates cells between guard cells, spacing out stomata. Symmetrical division creates two abutting guard cells with no intervening spacing cell. Clustering also occurs where the pattern of guard cell placement has an error, and the two adjacent protoderm cells create guard cells on sections of cell wall immediately facing each other (see figure 1 Dow et al). This is a simplistic explanation, and for detail, see Ohashi-Ito and Bergmann (2006).

If the pattern of stomata placement map to tubercles, then, so long as the tissues under the stomata are raised or swollen, this may explain tubercles. Everett et al (2001) found that the loose gas-exchange tissues under stomata have the ability to swell with water after heavy rain. The water is not absorbed through the stomata themselves, it is water absorbed by the roots and pushed by vascular turgor pressure into the fruit. As the loose sub-stomatal cells become turgid with water, they act somewhat as a shock-absorber. About two hours after the rain the cells return to normal. This temporary cell expansion could hardly explain tubercles – especially as they are already laid down at the earliest time of fruit development, regardless of whether it is dry or wet at the time.

In addition, the number of stomata per square centimeter varies widely between cultivars. Hass, a genotype with prominent tubercles, has an average of 69 stomata per square centimeter, and Topa Topa, which has smooth skin, has about 442 (Schroeder (1950)). This is the opposite of what you would expect if stomata patterning was responsible for tubercles.

And as Schroeder also points out, for the most part, stomata on avocado fruit skin are level with the epidermal layer.

Schroeder showed that a cork cambium and corky tissues develop at the stylar end of the avocado fruit (commonly called the fruit base, as opposed to neck) in some genotypes. This is associated with breakdown and suberisation of the tissues under the stomata. So, while there can be swelling associated with corky sub-stomatal tissue, it is only at a late stage of fruit maturity.

Stomata heavily concentrated around the remnants of the flower style

Finally, stomata are highly concentrated at the stylar end, and in conditions where these suberise at maturity, they appear to coalesce into a general corkiness of the base. The corkiness in no way resembles tubercles, and is localised to the base. In spite of the high local concentration of stomata, the base is no more tuberculated than the rest of the skin – and sometimes is less so, especially in the immediate vicinity of the stylar scar.

That’s it for the ‘stomatal tissue patterning’ hypothesis for tubercle development – or so it seems.

Rathod et al (2019) investigated the cause of both the tubercles and the ridges characteristic of the fruit of bitter gourd, Momordica charantia. They found that both phenomena were under single gene control. One gene, Tb, controls tubercles, and another, Cr, controls whether ridges are discontinuous, rather than continuous.

In cucumber, Cucumis sativa, a functionally identical gene (isofunctional homologue) also causing tubercles is labelled Tu (CsTu).

The Tb gene.

Crosses of smooth-skinned and ‘warty’ (tuberculate) genotypes of bitter gourd showed tuberculate to be dominant over smooth (Kole et al 2012). Similarly, the discontinuous ridge character state (Cr) was found to be dominant over continuous ridges (cr).

A Tb – like gene in avocado

An avocado isofunctional homolog of this gene would explain the surface topography of avocado fruit. It is also permissive of some association with the gene/s associated with stomata patterning (if so, this would be pleasantly tidy).

The variation in expression of tubercle height in avocado plants might be the result of the Tb gene being additive. A cross between a tuberculate cultivar and a cultivar that has a smooth skin as a result of a mutation that prevents Tb expression (tb mutant) fits nicely with this scenario, and Sonia Rios’s presentation of a smooth sector chimera in a tuberculate avocado fruit provides convincing evidence.

Selfed Hass seedlings show both markedly tuberculate progeny, and progeny with nearly smooth skin (Bergh and Whitsell 1973). If Tb was dominant in avocado, all the progeny would have had markedly tuberculate skin.

This result would be explained if Hass was heterozygous for Tb (Tb/tb). Absent modification by other genes, Tb/tb x Tb/tb ‘should’ give one Tb homozygote with markedly rough skinned seedling and one tb homozygote with apparently smooth skin to every two heterozygotes with intermediate skin pebbling.

In contrast to Hass, Fuerte has relatively small and low tubercles. But Bergh and Whitsell (1974) record that “many” selfed Fuerte seedling have “warty” skin, which suggests Fuerte, too, is a heterozygote for this character.

But why does Hass express the Tb gene so strongly if it is a heterozygote with only one active copy of the gene?

There may be other genes that further modify Tb expression.

How the Tb gene might work in avocado

Yang et al (2014) discovered that in cucumber, the Tu gene codes for a transcription factor (a C2H2 zinc finger protein) that ‘probably’ promotes cytokinin biosynthesis in the tissue that ultimately became tubercles. This transcription factor is further enhanced by another gene, Tsl, which affects the ultimate size of tubercles.

Tubercle size – the Ts1 gene

The specific gene (Ts1) listed in Wang et al 2020 (supplementary file 1) that specifies cucumber tubercle size codes for an oleosin protein, and is a promoter of gene expression. There are low levels of Ts1 expression in cucumbers without warts, or with small warts, and high levels of expression in those cultivars and lines with greater tubercle size (Yang et al 2019).

This heritable variation in tubercle size due to expression of the Tsl gene has a strong appeal as a plausible cause of variability in tubercle size in heterozygote avocado cultivars.

Some avocado cultivars, and Maluma is a good example, are extremely tuberculate. This is exaggerated at the immature stage.

Left, seedling showing low tubercle expression, right Maluma immature fruit with ‘hyper-expression’

This kind of ‘hyper-expression’ may well be due to even further epigenetic influences that enhance tubercle size.

Within-fruit localised tubercle over-expression

Avocado fruit – or at least pyriform avocado fruit – are asymmetrical. If you stand an avocado up on its base it may look symmetrical, but in fact the morphological ‘true’ base point of the fruit, at the floral scar (stylar scar, strictly speaking), is shifted up the side of the fruit, away from the apparent base (Cummings and Schroeder, 1942; see Fig. 12). The stylar scar, the ‘true’ halfway point, is marked with a yellow pin in the photo of the late season Hass fruit below. In other words, one side of the fruit is ‘smeared around the bottom of the fruit, visually at the expense of the other half.

The ‘apparent’ short (left hand) side of this Hass is has about the same perimeter distance as the other side.

The fruit stalk is attached offset from the apex in many pyriform cultivars, and viewed from the bottom of the stalk to the apparent base, this creates an apparent ‘short side’. The apparent short side meridial sector has significantly greater tubercle expression than the rest of the fruit surface, especially the apparent ‘long’ side. The ‘long’ side has rather flattened tubercles, which becomes more marked as the fruit enlarges and matures.

But the perimeter of the botanically accurate sides, measured from the pedicel core to the stylar scar, are almost identical in the above illustrated mature Hass fruit. The more heavily tuberculated ‘short side has a perimeter of 124 mm, and the ‘long’ side is 127 mm. Of course this is only one measurement and one cultivar.

For clues as to why side of the fruit might be more heavily tuberculated, we can look to the internal morphology of the fruit, which is well described in Cummings and Schroeder, 1942. In short, one half, the apparent short side has more and better vasculature, and is in contact with the seed as it develops. The apparent short side is more important to the plant for this very reason – it feeds the seed, it is the pipeline to the tree.

In contrast, the apparent ‘long’ side had fewer ‘pipes’, thinner ‘pipes’, and its vasculature terminates at the floral scar (or ends blindly), and doesn’t enter the seed at all (Cummings and Schroeder, 1942).

It is plausible that both endogenous hormones from the tree and locally produced phytohormones are delivered more quickly and more efficiently to the apparent short side, increasing signal concentration, and ‘pumping up’ tubercles locally. In the meantime, the infrastructurally depauperate apparent long side is short-changed in phytohormone supply and has reduced tubercle expression as a result.

This leaves still open the questions of which tissues initiate tubercle formation, and what exactly is a tubercle anyway.

What are tubercles?

Yang et al (2014) showed that in cucumber, tubercle initiation starts two days before flowering and continues until thirteen days after flowering. Tubercles develop due to localised rapid cell division. But it isn’t epidermal cells that develop into tubercles, spine cells do. Tubercles develop directly below the layer of spine cells. See Yang et al‘s (2014) paper for details.

Site of gene expression

Yang et al‘s (2014) work confirmed that in the crucial tubercle initiation stage 2 days before flowering, the cucumber Tu gene was not expressed in the epidermal tissues, nor in the tubercle tissues, but only in the basal cell layers of the spine. However, Ts1 which interacts with the Tu gene is expressed in tubercles, epidermis and pulp adjacent to the epidermis (Yang et al 2019). This implies signalling by a phytohormone. Cytokinin, involved in cell proliferation and differentiation is a good candidate.

The authors observed that the smooth skinned cucumber lines had small, fine spines (really a specialised form of trichome), whereas the ‘warty’ lines had large robust spines.

But avocado fruit don’t appear to have spines, remnant or not, as far as my x20 eyeglass allows me to see (although Wang et al 2020 mention what they call a “micro-trichome”(mict) mutant that shows no visible trichomes on fruit). Schroeder (1950), who examined the skin morphology in detail, makes no mention of hairs, spines or structures atop of tubercles. Everett et al describes lenticels, but makes no mention of spines.

Avocado don’t seem to have spines, and are therefore absent the layer of spine basal tissue that proliferates to form tubercles. But they do have areas of tissue proliferation on the skin. These areas of initially undifferentiated cells are the meristemoid tissues that are triggered to go on to form stomata in a patterned manner.

A speculative mechanism of tubercle origin in avocado

Mutations in the stomata precursor cells cause poorly controlled cell division, forming, in some cases ‘epidermal ‘tumors’ of guard cells (see Fig.2 (C) of Ohashi-Ito and Bergmann (2006) for an example in Arabidopsis leaf). The pattern, or map of the way stomata ‘should’ appear is also disturbed.

It is plausible that in avocado a similar series of mutations in cell proliferation and mapping might result in a clustered pattern of stomata whose underlaying tissues and adjacent cells have receptors sensitive to cytokinins (and maybe auxins). The cytokinins then cause proliferation of cells, and therefore tubercles. At some point the complex hierarchy of gene feedback then down-regulates promoters, cytokinin levels fall away, and tubercle growth stops.

What selective advantage do tuberculate fruit have over non tuberculate fruit?

There might be biomechanical advantages if tubercles ‘flatten’ with swelling fruit. Sudden increases in turgor after heavy rain can cause fruit skin cracking. A combination of cutin deposits in the epidermis (perhaps for tensile strength), sclerenchyma for skin thickness, and tubercles for flexibility might prevent premature cracking and fruit drop. The seed can then reach full maturity with maximal reserves in the cotyledons.

But avocado seeds are usually viable a long before full natural tree ripeness, so this seems a weak argument.

So far, I see no satisfactory explanation.


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