Christopher A. Clark
My research is primarily
directed at solving short and long-term disease problems of
the Louisiana and U.S. sweetpotato industries as well as
research aimed at better understanding the biology of
sweetpotato pathogens and diseases they cause. Efforts
currently emphasize two problems: the role of viruses in
cultivar decline, and efforts to improve postharvest disease
control with reduced reliance on prophylactic use of
Role of viruses in
sweetpotato cultivar decline
It has long been recognized
that sweetpotato cultivars decline in yield and quality
performance over years after they are released and even the
most popular cultivars are replaced about every 15-20
years. The reasons for this decline have not been well
defined but it is thought that accumulation of viruses
and/or mutations in the planting stock is responsible.
Although sweetpotato is the seventh most important food crop
worldwide and an economically important crop in a few states
in the U.S., including Louisiana, it has not received the
same research attention that many other crops have enjoyed.
As a result of limited investment in research, our
understanding of the viruses that infect this crop lags well
behind that for many other vegetatively propagated crops.
For many years, Sweet potato feathery mottle virus (SPFMV)
was the only virus recognized to occur in sweetpotatoes in
the U.S. However, our field studies indicate that SPFMV by
itself has minimal effect on yield of sweetpotatoes, even
though it re-infects healthy plants in the field very
rapidly. Therefore, our research has been directed in part
to determine what pathogens might be interacting with SPFMV
to cause cultivar decline. About 10 years ago, we found
that two other potyviruses, Sweet potato virus G (SPVG) and
Sweet potato virus 2 (SPV2) also occur commonly in
sweetpotatoes in the southeastern U.S. (Souto et al.,
2003). More recently, Sweet potato virus C has been
recognized as a distinct potyvirus species that is also a
common component of the virus complex. The
whitefly-transmitted begomoviruses, Sweet potato leaf curl
virus (SPLCV) and Sweet potato leaf curl Georgia virus, were
found to occur in ornamental sweetpotatoes and some
sweetpotato breeding lines. In field plot studies conducted
in 2000-2006, none of the virus combinations tested (SPFMV,
SPVG, SPV2, SPLCV) produced the same yield depression
obtained when using ‘naturally infected’ plants from
farmers’ fields as inoculum (Clark and Hoy, 2006). Studies
are in progress to determine whether adding SPVC to the
complex reproduces this yield effect.
Furthermore, when titers of
viruses were determined using real-time quantitative PCR
(Kokkinos and Clark, 2006), naturally infected plants had
about 200-fold greater titers of SPFMV, SPVG, and SPV2 than
artificially inoculated Beauregard plants grown under the
Relative titers of Sweet
potato feathery mottle virus (SPFMV), Sweet potato virus G (SPVG),
and Sweet potato virus 2 (SPV-2) as determined by
quantitative real-time PCR. ‘Artificial’ = plants graft
inoculated with all three viruses, ‘Natural’ = plants
exposed to infection in the field for 7 years. Plants
sampled for the test were grown in the same greenhouse
infected plants also have more severe and persistent
symptoms than plants artificially inoculated with SPFMV,
SPVG, and SPV-2:
Left = Beauregard
sweetpotato graft inoculated with SPFMV, SPVG, and SPV-2
showing virtually no symptoms, right = Beauregard plant
derived from a source that had been exposed to natural
infection in the field for 7 years.
It now appears that
sweetpotatoes are affected by a complex of viruses in the
U.S. that is not yet fully characterized. Effects on the
crop are likely determined by the interactions among these
viruses with their host and the timing of infection. We are
continuing to try and isolate and identify viruses from
sweetpotato with the intention of determining which ones are
critical to cultivar decline.
a service to the sweetpotato industry, we do meristem-tip
culture for virus therapy and subsequent indexing to produce
virus-tested plants of important cultivars and advanced
breeding lines from the LSU AgCenter breeding program.
These virus-tested plants are provided directly or through a
private company, Certis USA, to the foundation seed programs
and Alabama. Sweetpotato producers now have access to
relatively clean planting material, but they must usually
increase it on their own farms for at least one year before
they have sufficient seed to plant their crop. Re-infection
with SPFMV can be very high (often 100%) during this first
year on farms, so in collaboration with Drs. Tara Smith and
Don Ferrin, we conducted a multi-year
to determine the performance of sweetpotato seed from
farmers’ programs to determine when it is necessary for them
to replace their seed with foundation seed.
Everlyne Wosula’s PhD
research provided a lot of information about the
relationships among aphid vectors, potyviruses, and spread
of viruses in sweetpotato crops. A key finding of practical
significance is that potyvirus spread occurred primarily
during a 3-4 week period at about the time sweetpotato vines
are rapidly growing in the field, which coincides with a
peak of titer, especially of SPFMV. She also surveyed the
aphids in sweetpotato fields, determined the relative
transmission efficiency of the most common aphids: Aphis gossypii, Rhopalosiphum padi, and
Myzus persicae, and found
that common morning glory species were actually better
acquisition hosts for SPFMV than sweetpotato. Future
research in collaboration with
Dr. Jeff Davis in the Entomology Department will
endeavor to expand on this information to identify
strategies to reduce re-infection of virus-tested
sweetpotatoes in the field.
management of Rhizopus soft rot
Zygomycete that causes Rhizopus soft rot on sweetpotato, Rhizopus stolonifer, is an ubiquitous organism.
Rhizopus soft rot develops on sweetpotatoes that have been
cured and stored, infection occurring through wounds that
are incurred during the process of packing the storage roots
for shipment to market. It can completely decay roots in
1-2 weeks and for this reason, packers have routinely used a
fungicide, primarily dicloran (Botran®) applied to the roots
after they are washed to control the disease. Since sweetpotato is the most popular baby food and
since it is also popular with people trying to follow a
health-conscious diet, reliance on prophylactic application
of a fungicide at the last stage in packing is undesirable.
We are therefore doing research to try and develop an
integrated management approach to improve management of
Rhizopus soft rot while reducing reliance on fungicides.
is often used for managing diseases, but there had been
little effort to investigate resistance to postharvest
diseases, especially in sweetpotato. We developed methods
for screening for Rhizopus soft rot resistance and found
that Beauregard, the dominant cultivar in U.S. production
from 1988-2008 had greater resistance than earlier cultivars
(Clark and Hoy, 1994). However, despite its resistance,
Rhizopus soft rot can still occur on Beauregard, and we are
working with Dr. Don LaBonte to develop lines with greater
levels of resistance that are horticulturally acceptable.
Sweetpotato IPM Project was funded from 2003-2007 by the
USDA Risk Avoidance and Mitigation Program (RAMP) and Gerber
Foods that involved plant pathologists and entomologists
from the LSU AgCenter, North Carolina State University,
Mississippi State University, and Auburn University in a
major program to address problems with soil insects and
postharvest diseases. Factors investigated in relation to
Rhizopus soft rot included the role of wounds incurred on
packing lines, the effect of postharvest environment, and
the effect of preharvest environmental factors and cultural
practices on disease.
was conducted in plots in over 20 fields per year on
commercial sweetpotato farms in Louisiana, and a similar
number were conducted by colleagues in North Carolina, all
growing Beauregard. Sweetpotatoes harvested from these
plots were cured for 5 days, then stored at 60oF
for 100-120 days and inoculated with R. stolonifer
and Dickeya didantii (syn. Erwinia chrysanthemi)
using standardized wounding techniques and uniform inoculum.
Data was also collected from each of these plots for various
weather parameters, soil analyses, and cultural practices
followed by the producer. The results indicated that
differences in the preharvest environment have dramatic
effects on susceptibility of Beauregard sweetpotatoes to
both diseases, but also indicates that the two diseases
respond differently to the environment.
Incidence of Rhizopus soft
rot and Bacterial soft rot in Beauregard sweetpotatoes
harvested from 21 different fields in Louisiana in 2006.
The roots were cured, stored, and inoculated under identical
Various statistical analyses of the data from
these plots indicated that certain weather variables such as
soil and air temperature and soil moisture and soil
constituents such as calcium, phosphorus, potassium, and
organic matter may influence susceptibility of Beauregard to
Rhizopus soft rot. Research is ongoing to verify the role
of these variables and determine their interactions. Dr.
Arthur Villordon at the Sweet Potato Research Station has
used the yield data from the same plots to help develop a
growing degree day model for determining optimal harvest
time of sweetpotato and is working on a model to determine
optimal planting time. Eventually, we would like to combine
these into a production model that producers can use to best
manage their practices.
are evaluating other materials and practices that can be
used on packing lines to reduce Rhizopus soft rot. This
includes evaluation of commercial ‘reduced risk’ fungicides
and biological controls. We have also worked with Dr. Dave
Picha to evaluate the potential for using hot water. While
some experiments indicated that hot water (52-54oC
for 2-4 mins.) significantly reduced Rhizopus soft rot
incidence, in some experiments, hot water treatments
increased Rhizopus soft rot. Planned studies will address
how environmental variables, hot water treatments, and
post-packing treatments affect wound healing of
sweetpotatoes and Rhizopus soft rot susceptibility.
Streptomyces soil rot
soil rot disease, which is caused by the soil-borne
actinomycete, Streptomyces ipomoeae was the most
significant disease problem on sweetpotatoes in the U.S.
prior to the development of resistant cultivars by the LSU
AgCenter. Early on we determined that this pathogen is one
of very few prokaryotic pathogens with the ability to
directly penetrate plants (Clark and Matthews, 1987). We
also found that strains of this pathogen collected from
various locations in the U.S. and Japan were relatively
homogeneous when compared using rep-PCR and plasmid
profiling (Clark et al., 1998). However, they could be
divided into three groups based on inhibitory interaction
in the Department of Biological Sciences has an interest in
molecular biology of Streptomyces species and taken
this area of research into a molecular study of the
inhibitory phenomena that involve production of a
bacteriocin-like substance, ipomicin and is actively
investigating the mechanisms of pathogenicity in this
AgCenter sweetpotato breeding program is a highly productive
team effort involving scientists in the School of Plant,
Environmental, and Soil Sciences, the Sweet Potato Research
Station, and the Departments of Plant Pathology & Crop
Physiology and Entomology. Breeding lines from this program
are screened for resistance to multiple diseases including
Streptomyces soil rot, Fusarium wilt, internal cork,
root-knot nematode, bacterial root and stem rot, Fusarium
root rot, and others. The LSU AgCenter program has been
the primary source of resistance to Streptomyces soil rot
and has released a number of cultivars, some of which have
been very widely adopted by the industry. The most notable
example is Beauregard which accounted for >80% of U.S.
sweetpotato acreage during the period 1988-2006. Since
1980, the following cultivars have been released all of
which are resistant to Fusarium wilt and Streptomyces soil
rot and have other disease resistance as well:
1980 - Travis (L74-62)
- grown on limited acreage in LA for several years
1981 - Eureka (L74-131)
- grown on limited acreage in CA for several years
1987 - Beauregard
(L82-508) - grown on approx. 80% of US acreage
1990-2005, also grown in Australia and New Zealand.
1992 - Hernandez
(L82-66) - grown on approx. 5-10% of US acreage since
1995, mostly in NC
1994 - L86-33 - used as
a source of multiple disease and pest resistance in U.S.
and international breeding programs
1995 - Darby (L87-59) -
not grown commercially to any significant extent
2001 - L96-117 - Patent
No. US PP 15,038 P2 awarded to LaBonte, D., Wilson, P.,
Clark, C., Villordon, A., and Cannon, J.
2002 - Bienville
(L94-96) - Patent No. US PP 15,580 P3 awarded to LaBonte,
D., Wilson, P., Clark, C., Villordon, A., Cannon, J.,
Story, R., and Hammond, A.
2007 - Evangeline
(L99-35) – U. S. Patent Ser. No. 11/789,681 awarded to
LaBonte, D., Villordon, A., Clark, C.
2007 - Muraski-29
(L01-29) – U. S. Patent Ser. No. 11/975,203 awarded to
LaBonte, D., Villordon, A., Clark, C.
2011 – Bonita (L05-29)
– Patent No. US PP22,719P3 issued to D. R. LaBonte, A.
Q. Villordon, T. P. Smith, and C. A. Clark.
2012 – Orleans
(L05-111) – Patent No. US PP23,761 issued to D. R.
LaBonte, A. Q. Villordon, T. Smith, and C. Clark
2012 – 07-146 – Patent
No. US PP23,785 P3 issued to D. R. LaBonte, A. Q.
Villordon, T. Smith, and C. A. Clark
Left = the susceptible
cultivar Centennial, and right = a resistant breeding line
growing in the Streptomyces soil rot nursery.