The “Apogee effect” – examination of the mode of action of prohexadione calcium in shoot blight cont

Studies of the mechanism of action of Apogee reveal that this growth inhibition results in the production of a physical barrier (thickened cell walls) to infection by the fire blight pathogen.

Apogee (prohexadione-calcium; BASF) is a growth inhibitor that we have known for years to provide excellent control of the shoot blight phase of fire blight. This article provides information on research results from my lab at Michigan State University aimed at determining the mechanism of action of Apogee in shoot blight control. For those mostly interested in suggestions for Apogee use for apple in 2012, see my accompanying article, “Use of Apogee for shoot blight control in 2012.”

My lab has worked on determining the mechanism of action of Apogee in shoot blight control for the last several years. First, we eliminated the possibility that Apogee induced the tree to produce compounds inhibitory to the fire blight pathogen. Ultimately, we began assessing the possibility that Apogee induces trees to produce a physical barrier to fire blight infection.

We began examining cell walls in leaves taken from shoot tips of ‘Gala’ trees either treated with or not treated with Apogee at a high rate (12 oz / 100 gallons). The “Apogee effect” on shoot blight control becomes apparent approximately 10 to 14 days after application. We analyzed leaf cross-sections using conventional microscopy and scanning electron microscopy (SEM). The SEM studies allowed us to obtain a close-up view of what was happening at the shoot tip. What we consistently observed were cotrical parenchymal cells from Apogee-treated shoots with thickened cell walls compared to those from non-treated shoots (Figure 1). The red arrows in panels A and B (Apogee-treated) denote areas of cells with thickened cell walls, while the red arrow in panel C points to a comparable area from a non-treated leaf. In addition, most of the Apogee-treated leaves also contained additional areas or “layers” of material surrounding the vascular tissue (yellow arrows).

Figure 1. Cross-sections of ‘Gala’ leaf midveins enabling
a visual examination of cell walls from Apogee-treated
(A and B) and non-treated (C) leaves.
Panel A
Panel B
Panel C

We measured the width of thousands of cell walls from leaf midvein cortical parenchmyal tissue and found some interesting results (Table 1). Cell wall widths from the tips of the youngest leaf of the shoot averaged 1.17 µm compared to 2.36 µm from Apogee-treated leaves. For reference, 1.17 µm = 0.000117 cm = 0.000046 inches. Thus, Apogee treatment doubled the cell wall width! Granted, this doesn’t sound like much, but from the perspective of the fire blight bacterium, it is huge.

Table 1. Effect of prohexadione-calcium (Apogee) on the width of cell walls of the midvein cortical parenchyma tissue of apple cv. ’Gala’. Cell wall widths greater than 2 µm are highlighted in bold.


 Midvein cell wall widths (µm) with standard error

 Location of veinal section from leaf tip

0.5 cm


2 cm

 Sampling date (days after treatment)

Leafa

Treatment

7 d

13 d


7 d

13 d

1st

Non-trt

0.90 ± 0.10 cb

1.17 ± 0.11 c


1.64 ± 0.11 c

2.04 ± 0.16 c


Apogee

1.67 ± 0.07 a

2.36 ± 0.07 a


2.26 ± 0.30 b

2.97 ± 0.18 a








2nd

Non-trt

0.97 ± 0.02 c

1.82 ± 0.12 c


1.65 ± 0.13 c

1.92 ± 0.03 c


Apogee

1.85 ± 0.05 a

2.56 ± 0.08 b


1.91 ± 0.06 b

2.90 ± 0.06 a








7th

Non-trt

1.89 ± 0.03 a

2.04 ± 0.01 c


2.51 ± 0.05 a

2.22 ± 0.02 b


Apogee

1.92 ± 0.08 a

2.49 ± 0.19 a


2.59 ± 0.06 a

2.82 ± 0.05 a

a The 1st, 2nd, and 7th youngest unfolded leaves were sampled from shoots.
b
Differences among treatments/leaf/sampling date/location from leaf tip were determined using the Kruskal-Wallis test followed by the post-hoc Games-Howell multiple comparison test when P ≤ 0.05. Different letters (for each treatment/leaf/sampling date/location) indicates significant differences (P ≤ 0.05).

Bacterial pathogens such as the fire blight pathogen produce a needle-like apparatus that they use to cause disease. From other lab research that we’ve done, we know that the fire blight pathogen must infect living cells prior to gaining access to the plant xylem and moving systemically through the tree. The needle-like apparatus necessary for disease was examined by Dr. Sheng Yang He’s group at MSU and found to be approximately 2 µm long. An examination of the data shown in Table 1 indicates that Apogee-treated cell walls all exceed 2 µm in width on average. This suggests that the bacterial needle is not long enough to cross the plant cell wall and allow infection to proceed. We believe that this cell wall physical barrier provides the mechanistic basis for shoot blight control.

Note a few other points from the data presented in Table 1. Cell walls are, on average, thicker in older leaves, even in the second leaf at the shoot tip. Cell walls are also thicker 2 cm (0.8 inch) from the tip of a leaf compared to 0.5 cm (0.2 inch). Even the cell walls of non-treated leaves have widths greater than 2 µm in the seventh leaf from the shoot tip. This correlates well with our physical barrier hypothesis as these older leaves on shoots are seldom infected by the fire blight pathogen. Finally, the width of cell walls is not quite thick enough at seven days following Apogee treatment. This also correlates with our knowledge that it takes approximately 10-14 days after application for the “Apogee effect” to become apparent.

In particular with highly-susceptible cultivars, Apogee remains our best option for fire blight shoot blight management and has many times helped avoid epidemic outbreaks. Furthermore, it should be remembered that Apogee treatment controls both streptomycin-resistant and streptomycin-sensitive strains of the fire blight pathogen.

Dr. Sundin’s work is funded in part by MSU‘s AgBioResearch.

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