PGRs affect turf-disease management

Plant growth regulators (PGRs) have been in use for many years, but we still have relatively little information about how they affect turf-disease management. Earlier work suggested that disease symptoms were more severe in PGR-treated turf. However, researchers recently have been studying several of the newer PGRs and, in general, their effects do not diminish our ability to manage turf diseases. In fact, some even have fungistatic activity. Nevertheless, a review of the research conducted to date on PGRs suggests that products' effects vary, and we, therefore, must consider each PGR individually to determine if it will improve or diminish turf-management goals, including disease management.

PGR types PGRs affect plants by either increasing rates of growth or development or, more commonly, by inhibiting or suppressing growth or development. (Growth is an increase in cell number or size, and development is the process of specialization leading to the formation of tissues, such as leaves, shoots or rhizomes). PGRs act by interfering with meristems--the actively dividing group of cells in the crowns, rhizomes and stolons of grass plants that are responsible for most growth and development.

Scientists divide PGRs into two basic types: Type I and Type II.

* Type I PGRs. Type I compounds have the ability to inhibit or suppress both growth and development. Thus, for example, they may prevent flowering in addition to reducing growth. We can separate Type I PGRs into two groups:

*Inhibitors. Chemicals such as maleic hydrazide, chlorflurenol and mefluidide (see table below for a listing of brand names of PGRs that are currently available for turfgrass use) inhibit foliage and seedhead development of cool-season grasses. These compounds rapidly stop cell division and differentiation in meristematic tissues and are mainly foliar-absorbed (chlorflurenol also is absorbed by roots). You may observe suppression of turf growth, including initiation of new leaves, within 1 week of an application, and this suppression can last from 4 to 10 weeks.

*Suppressors. We characterize the second group as growth suppressors. These compounds are not the same as inhibitors due to their different site of absorption (roots) and mode of action. Absorption via the roots occurs more slowly than through foliage. Thus, more time passes before inhibition compared to foliar-absorbed products. In most cases, then, growth doesn't immediately cease (as with inhibition) but rather is merely suppressed. However, at least one suppressor, amidochlor, can completely stop growth. EPTC is another example of a suppressor. Both amidochlor and EPTC provide foliar suppression for approximately 6 weeks following a single application.

*Type II PGRs. Type II PGRs inhibit the growth of the plant but do not interfere with its developmental processes, as do the Type I PGRs. This results in continued development of new plant organs that are smaller but normal in structure. Type II chemicals, such as flurprimidol, paclobutrazol, tri-nexapac-ethyl and uniconazole, suppress plant growth by inhibiting gibberellin synthesis. These compounds are mainly root-absorbed with the exception of trinexapac-ethyl, which--unique to the available Type II PGRs--is foliar-absorbed. Type II PGRs can provide foliar suppression 3 to 4 weeks longer than Type I PGRs. Due to their site of uptake and mode of action, Type II PGRs generally are less phytotoxic than some Type I products and you can overlap applications with less potential for injury. While Type II PGRs all inhibit gibberellin synthesis, they do so through a variety of modes of action.

Paclobutrazol and flurprimidol are chemically related to certain fungistatic compounds, while trinexapac-ethyl is not and exhibits little fungistatic activity. Paclobutrazol is a triazole and, as such, is structurally related to several important turf fungicides.

Research on Type I PGRs and turfgrass disease All turf-management practices can affect your disease-management goals. Some of these interactions can lead to reduced resistance, survival, rate of recovery and recuperative potential of turf. Thus, it is important to consider all of your turf-management practices when developing your disease-management program. PGRs are one of the management inputs that can affect disease management.

Keep in mind that PGRs have been around for more than 40 years and have not caused any major disease problems in turf. However, that does not mean that they have no effects at all. Observations by both turf managers and researchers suggest that some PGRs may change turf-disease severity.

Before the mid-1990s, most knowledge about PGR-turfgrass-disease interactions related to either maleic hydrazide (MH) or mefluidide, both Type I PGRs. The results of these older studies include:

*MH applications for controlling vegetation along fence lines for 2 consecutive years caused an increase in the level of infestation and size of rust pustules on reed canarygrass and smooth bromegrass.

*Single applications of MH, at several different rates, caused severe rust infestations in 'Kentucky 31' tall fescue.

*Experimental PGRs that researchers applied to the same plots for 2 consecutive years produced minimal effects on foliar growth and seedhead development of 'Manhattan' perennial ryegrass, but severely retarded root development. In addition, turf treated with MH developed red thread.

*MH and mefluidide, used alone and in combination with broadleaf herbicides, fungicides and surfactants on a variety of cool-season species and cultivars caused severe red-leaf-spot lesions, while untreated turf was almost symptomless.

*Plots of 'Newport' or 'Fylking' Kentucky bluegrass or 'Kentucky 31' tall fescue treated with mefluidide developed patches of red thread.

*Kentucky bluegrass and tall fescue treated with mefluidide and MBR18337 (an experimental compound) developed severe "Helminthosporium" leaf spot, and untreated plots did not. In the same study, other experimental PGRs had no effect on disease severity.

*In a 2-year study looking at repeated applications of mefluidide, MBR 18337, EL 72500 (another then-experimental material) and ethephon on Kentucky bluegrass, treated plants exhibited the highest percentage of leaves bearing Drechslera poae leaf-spot lesions. However, the effects were rate-dependent. Turf treated with EL 72500 showed the lowest percentage of leaves bearing leaf-spot lesions of all the treatments.

*Mefluidide and Sustar (an agricultural PGR) applied a single time to 'Pennstar' and 'Fylking' Kentucky-bluegrass stands did not affect dollar-spot development (which occurred in all plots--treated and untreated). In the same study, however, turf treated with these materials suffered more severe stripe-smut and leaf-spot lesions than untreated turf. The researchers suggested that the disease appeared worse in these plots because the treatments suppressed new growth. Thus, the turf remained short, and mowing did not remove the symptoms.

(Editor's note: mefluidide's current label, as PBI/Gordon's Embark brand, specifies rates considerably lower than label rates that were current when the studies cited above took place [mefluidide was a 3M product prior to 1989]. Thus, it is probable, depending on rates used in specific studies, that the effects noted were much more pronounced than would occur with current, lower rates.)

Research on Type II PGRs In the mid-1990s, we conducted a study at the University of Illinois, as did Dr. Lee Burpee at the University of Georgia, to determine if, and how, three Type II PGRs--paclobutrazol, flurprimidol and trinexapac-ethyl--interacted with dollar spot and brown patch on creeping bentgrass maintained as a golf green.

*Dollar spot. Both studies considered dollar spot. In the Georgia study, paclobutrazol acted as a fungistat (it prevents the spread of, but does not kill, fungi), and its reduction of turf growth did not appear to interfere significantly with dollar-spot management. Further, Dr. Burpee suggested that pre-treatment with paclobutrazol could improve the subsequent performance of some fungicides against dollar spot. Flurprimidol behaved similar to paclobutrazol (in both studies) in that it was fungistatic and improved fungicidal control of dollar spot. Trinexapac-ethyl was only weakly fungistatic in the laboratory, but in the field it reduced disease severity of treated turf and enhanced the performance of fungicides.

*Brown patch. In the laboratory, we found that flurprimidol inhibited the growth of Rhizoctonia solani while trinexapac-ethyl was weakly fungistatic. In the field, however, bentgrass treated with trinexapac-ethyl had less-severe brown patch compared to turf treated with flurprimidol. We did not test paclobutrazol on brown patch and Dr. Burpee's study did not consider brown patch at all.

What was interesting in both the Illinois and Georgia studies was that disease severity did not seem to become worse or more prolonged by the use of PGRs, in spite of the reduced growth of the turfgrass.

Turf-disease management: A two-part process The results of studies to date support several concepts that pathologists understand about turf-disease management:

*Disease management is a combination of controlling pathogen growth and promoting plant growth.

*Each individual chemical we use on turf has unique effects on non-target organisms, which we need to study to better understand the consequences of their use.

*PGR compounds with fungicidal properties will behave as fungicides when you apply them to turf.

*Turf management is an integration of practices, and disease management is only one part of the total program.

The plain, but unfortunate, truth about diseased crowns, shoots and leaves is that they do not recover. Fungicides can prevent additional infections from occurring and spreading, but infected portions of the plant are lost. Fortunately, grass plants, especially those we use for turf, can regrow new parts, thus surviving the infection as long as some crowns are viable. The plant will put forth new, healthy leaves and shoots, compensating for the lost tissue. However, the old, infected parts remain, and the only way to remove them is to mow them off.

By far the most important concept that we can leave you with is: Turf-disease management is a two-part process. Slow or stop the growth of the pathogenic fungus and support turf growth. One without the other will not work. With this simple model for managing disease in mind, let's sum up how PGRs can affect turf disease.

PGRs can have both direct and indirect effects. Some PGRs can directly reduce the population or activity of a fungal pathogen in ways similar to fungicides, which control turf diseases by blocking the fungi from attacking and causing lesions. (As we mentioned earlier, some PGRs have chemical structures similar to certain fungicides, so this is not surprising.)

Next, based on other studies (of crops other than turf), it's possible that PGRs may indirectly reduce natural suppression of pathogenic fungi by inhibiting beneficial fungi that live in the turf. Without them, pathogens have no competition and can more aggressively attack the turf, causing more severe disease.

Finally, PGRs reduce the growth of turf. This means that PGRs can slow the rate at which new tissue is able to replace old or diseased tissues. Thus, disease symptoms last longer in the turf.

PGRs comprise a wide range of chemicals, each with its own unique effects on turf. Although some PGRs are chemically similar to known fungicides and have some fungistatic activity, it is unlikely that they can replace the need for fungicides. It's interesting that treatment with certain PGRs before using a fungicide enhances the efficacy of the fungicide. Presently, we can offer no explanation for this.

Reducing the activity of fungal pathogens addresses half of the turf-management model: stop the pathogen. While PGRs do inhibit turfgrass growth, the magnitude of this effect--combined with the potential to suppress pathogen growth--does not appear to significantly prolong the recovery of moderately diseased turf (this may not be as true for severely diseased turf). Thus, the other half of the model--encouraging the turf to grow--is satisfied.

We still have a great deal to learn about the non-target effects of PGRs in a turf-management program. So far, however, research results support their continued use.

Henry T. Wilkinson and Thomas W. Fermanian are professors at the University of Illinois (Urbana-Champaign, Ill.). J.M. McMeans, formerly a graduate student at the University of Illinois, is currently pursuing her Ph.D. in plant molecular biology at Virginia Polytechnic Institute and State University (Blacksburg, Va.).

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