Pathogenicity of Phytophthora capsici Leon and Rhizoctonia solani Khün, on seedlings of ‘costeño’ pepper (Capsicum annuum L.)

D. Gómez-Hernández1; J. C. Carrillo-Rodríguez1; J. L. Chávez-Servia2*; C. Perales-Segovia3

1. Instituto Tecnológico del Valle de Oaxaca, Ex-hacienda de Nazareno, Santa Cruz Xoxocotlán, C.P. 71230, Oaxaca, México., Instituto Tecnológico del Valle de Oaxaca, Instituto Tecnológico del Valle de Oaxaca,

<postal-code>71230</postal-code>
<state>Oaxaca</state>
, Mexico , 2. Instituto Politécnico Nacional, CIIDIR-Oaxaca, Hornos Núm. 1003, Col. Noche Buena, Santa Cruz Xoxocotlán, C.P. 71230, Oaxaca México., Instituto Politécnico Nacional, Instituto Politécnico Nacional, CIIDIR,
<postal-code>71230</postal-code>
<state>Oaxaca</state>
, Mexico ,
3. Instituto Tecnológico El Llano, km. 18 Carr. Aguascalientes-San Luis Potosí, C.P. 20256, El Llano, Aguascalientes, México., Instituto Tecnológico El Llano, Instituto Tecnológico El Llano,
<postal-code>20256</postal-code>
<city>Llano</city>
<state>Aguascalientes</state>
, Mexico

Correspondence: *. Corresponding Author: Chávez-Servia, José Luis. Instituto Politécnico Nacional, CIIDIR-Oaxaca, Hornos Núm. 1003, Col. Noche Buena, Santa Cruz Xoxocotlán, C.P. 71230, Oaxaca México. E-mail: E-mail:


Abstract

For decades, there has been a need to continuously evaluate the Capsicum germplasm to identify sources of resistance to Phytophthora capsici and Rhizoctonia solani. The objective of this study was to evaluate the pathogenicity and severity of eight P. capsici isolates and two R. solani isolates in ‘costeño’ pepper seedlings (Capsicum annuum L.). Chile pepper plants exhibiting symptoms of wilt were collected from 11 communities in Oaxaca, and eight isolates of P. capsici and two of R. solani were obtained in the laboratory from diseased tissue. Of these isolates, two independent experiments were designed according to the pathogen using a randomized complete block design with three replicates in ‘costeño’ pepper seedlings that were previously germinated and inoculated 17 days after transplantation. Significant differences between the P. capsici inocula origin were observed for all the evaluated variables, and it was determined that once the seedling was invaded by the pathogen, it died in less than 21 days. Among the R. solani isolates, there were no significant differences in the damage variables, but they could cause seedling death in less than 15 days after inoculation. Regarding pathogenicity, the P. capsici isolates from San José El Progreso and San A. Castillo Velasco, Oaxaca, caused greater damage and seedling death in less than 10 days; thus, they are useful for identifying possible sources of tolerance among pepper populations. In R. solani, the isolates from San Sebastián Abasolo (RS7) and El Arrogante, Ejutla de Crespo (RS52) did not show significant differences in terms of virulence in the pepper seedlings.

Received: 2017 September 27; Accepted: 2018 March 6

revbio. 2020 May 31; 5: e356
doi: 10.15741/revbio.05.e356

Keywords: Keywords: Pathogenic isolates, pathogenic complex, pepper wilt, pathosystems.

Introduction

Chile pepper wilt is a difficult-to-control plant disease, and there are no simple methods or strategies that allow for the adequate control of the pathogen complex, which is composed of Phytophthora capsici, Rhizoctonia spp., Fusarium spp., Verticillium spp., Macrophomina spp., Pythium spp. and Screrotium rolfsii, among others (Ristaino & Johnston, 1999; Velásquez-Valle et al, 2001 and 2003; González-Pérez et al., 2004; Rico-Guerrero et al., 2004; Vásquez et al, 2009; Montero-Tavera et al., 2013). Each pathogen can act in isolation, although the presence of complexes is common. Among the most aggressive and pathogenic are Phytophthora capsici and Rhizoctonia solani. The presence of pathogen complexes makes it difficult to establish a specific epidemiological pattern, and as a result, several control strategies must be used (Montero-Tavera et al., 2013) because up to 100 % of losses can occur during chili pepper production.

R. solani is a soil-borne pathogen that is very aggressive to newly transplanted seedlings when there is excess moisture in the transplant soil or bed. It is a pathogen that causes damping off of seedlings, and its prevalence and incidence is high in fields and greenhouses and in vegetable crops with no crop rotations. This pathogen remains in soil after each crop growth cycle in both the parasitic and saprophytic stages with sexual and asexual reproduction. The mycelia or sclerotia created by asexual reproduction usually remain in infested soils, and these structures are the source of crop infections. They form dense masses of moniloid cells as a mechanism for protecting themselves against environmental changes by producing exudates composed of phenolic compounds, carboxylic acids, carbohydrates, fatty acids and amino acids, which help increase their fungal and phytotoxic activity (Aliferis & Jabaji, 2010; Zachow et al., 2011).

During the initial growth phase of seedlings, R. solani causes mortality close to 25 % of the crop, and it is usually associated with Pythium, which also causes wilt or damping off (González-Pérez et al., 2004) and damages up to 33 % of productive adult plants (Montero-Tavera et al., 2013). To date, several management strategies have been proposed for crops infested with R. solani, such as the use of bacteria of the Bacillus genus, among other microorganisms and chemical products. However, the results have been unfavorable (Velásquez-Valle et al., 2003; Guillén-Cruz et al., 2006).

P. capsici causes severe losses during Capsicum spp. production because it survives from crop cycle to crop cycle in residues from the previous crop in the form of oospores, which are resistant to drought and extreme climate variations for several years, even in the absence of host plants, and they later germinate with moisture (Banadoost, 2005). Severe infections cause root rot, strangulation of the stem base, yellowing, leaf shedding and plant death.

The lesions caused by P. capsici are overrun by other pathogenic oomycetes (Avelar & Marban, 1989; Velásquez-Valle et al., 2001). The planting soils overrun by this pathogen favor sexual and asexual reproduction, and therefore, they favor the presence of multiple pathogenic races. In Capsicum, up to 20 races of P. capsici have been identified; the most common races cause root rot and four induce leaf blights. In all cases, the sources of host resistance are controlled by multigene complexes (Lefebvre & Palloix, 1996; Oelke et al.., 2003; Sy et al., 2008). In addition to the diversity of pathogenic races, there is high variability in the virulence among isolates with the same geographic origin (Muhyi & Bosland, 1995; González-Pérez et al., 2004).

Despite the research carried out on this subject, the distribution and aggressiveness of different pathogen races of P. capsici, their genetic variability and the chemosensitivity that promote damage to the plant have not been documented (Bower et al., 2007; Meitz et al., 2010; Oh et al., 2010; Quesada- Ocampo et al., 2011;. Glosier et al., 2008; Sy et al., 2008). In addition, it is necessary to understand the behavior of pathogenic isolates and the variability in their infective potential (Quesada-Ocampo et al., 2011) and evaluate the identification of etiological patterns or resistance in germplasm in the laboratory or field (Montero-Tavera et al., 2013). In regional experiments to identify Capsicum resistance to pathogens that induce wilt, the isolates and pathogen races from the region will be released where the native plants or genetically improved material will be grown (Meitz et al., 2010; Moran-Bañuelos et al., 2010; Anaya-López et al., 2011; Pérez-Acevedo, 2014).

It is generally difficult to predict the pathogenic behavior of a race and its isolates because it depends on the variations in the environmental conditions, the aggressiveness of the pathogenic race or anastomotic group as well as the host plant growth conditions (Ristaino & Johnston, 1999). Therefore, it is necessary to evaluate the aggressiveness of P. capsici (Gil-Ortega et al., 1995; Black & Berke, 1998; Oelke et al., 2003; Glosier et al., 2008; Sy et al. 2008) and R. solani (Muhyi & Bosland, 1995; El-Abdean et al., 2013) by considering the different geographical origins of the isolates from each species. Thus, the pathogenicity and incidence of different Phytophthora capsici L. and Rhizoctonia solani isolates were evaluated in ‘costeño’ pepper (Capsicum annuum L.) seedlings in Oaxaca, Mexico.

Materials and Methods

Collection of plants with symptoms caused by P. capsici and R. solani

Plants damaged by P. capsici and R. solani were collected from 11 communities in the Central Valleys of Oaxaca (also known as the Oaxaca Valley; Table 1) between 16° 01’ and 17° 33’ N, 95° 58’ and 97° 30’ W, a region with an average annual temperature between 18 and 22 °C and 725 mm of average annual rainfall. The exploration and collection was designed based on previous studies that reported the presence of P. capsici and R. solani pathogenic isolates (Vásquez et al., 2009; Perez-Acevedo et al., 2017). Several ‘chile de agua’ pepper plants were collected from each community and were transported in plastic bags to the laboratory at the Instituto Tecnológico del Valle de Oaxaca.

Table 1.

Communities where were collected pepper plants with symptoms caused by P. capsici, and R. solani from the Valles Centrales of Oaxaca, May-August 2015.


Community Municipality Latitude (N) Longitude (W) Altitude (m.a.s.l)
Ejutla de Crespo El Arrogante, Ejutla de Crespo 16° 31′ 96° 41′ 1,550
San José El Progreso San José El Progreso 16° 41ʼ 96° 41ʼ 1,580
Ocotlán de Morelos Ocotlán de Morelos 16° 48ʼ 96° 40ʼ 1,500
Del Magdalena Teitipac Magdalena Teitipac 16° 54ʼ 96° 33ʼ 1,730
San Jerónimo Tlacochahuaya San Jerónimo Tlacochahuaya 17° 00ʼ 96° 09ʼ 1,180
Villa de Etla Villa de Etla 17° 12ʼ 96° 48ʼ 1,660
San Juan de Dios Reyes Etla 17° 12ʼ 96° 49ʼ 1,630
San A. Castillo Velasco San Jerónimo Taviche 16° 48ʼ 96° 41ʼ 1,480
El Carrizal Cuilapan de Guerrero 16° 59ʼ 96° 47ʼ 1,560

Isolation and multiplication of P. capsici and R. solani

From chili pepper plants damaged by P. capsici, 1-cm stem sections were cut, washed in running water and disinfected with 1.5 % sodium hypochlorite. They were then transferred to petri dishes containing PDA (potato, dextrose and agar) medium and V8® Juice (20 %), and they were incubated in a humidity chamber at room temperature under white light for 10 days. Once the growth was identified as P. capsici according to the keys by Romero-Cova (1988), the isolates were placed in new petri dishes to multiply. The release of the zoospores was induced by decreases in temperature for half an hour in a refrigerator at a temperature of 5 °C followed by one hour at room temperature, and this procedure was repeated four times. The concentration was adjusted to 25,000 zoospores m L-1 of water with the help of a Neubauer chamber.

For R. solani, RS-1 and RS-2 were used; these were obtained from diseased chili pepper plants from crops established in the Ejutla-Ocotlan region of Oaxaca. The isolates were cultivated in PDA for seven days at room temperature in the dark. Once the fungus that had been placed in the petri dishes had multiplied, 10 mL of water was added; the mycelium was subsequently removed with a spatula to make a homogeneous mixture and the solution was adjusted to a concentration of 90,000 fragments m M-1 of water with the help of the Neubauer chamber. This solution was used to inoculate the chili pepper seedlings.

Inoculation and evaluation of pathogenicity

To evaluate the pathogenicity of P. capsici and R. solani, a population of ‘costeño’ peppers (Capsicum annuum L.) was used. The sowing and seedling growth occurred from September to November 2015 in polystyrene trays containing Peat moss® substrate in the greenhouse at the Instituto Tecnológico del Valle de Oaxaca. When the seedlings had 4 to 6 true leaves, they were transplanted to 1-L Styrofoam pots with vermiculite (inert substrate), and they were watered with 15-30-15 Ultrasol fertilizer (initial stage). In both cases, the evaluations were made under a randomized complete block design with three repetitions and 12 seedlings as experimental units plus an uninoculated control. Eight isolates of P. capsici and two of R. solani were evaluated during independent experiments.

Seventeen days after transplantation, the plants were inoculated with P. capsici isolates that were previously prepared by adding 10 mL of a solution containing 25,000 zoospores/mL in distilled water to the base of the stem. The plants were subsequently irrigated to the daily field capacity to promote infection by the pathogen. The greenhouse temperature (22 to 36 °C) and relative humidity (42 to 100 %) readings in the greenhouse during the experiment are shown in Figure 1.


[Figure ID: f1] Figure 1.

Regimes of temperatures and relative humidity percentage (RH) during evaluation of damages by P. capsici and R. solani.


Twenty-eight days after the transplantation (6 true leaves), R. solani was inoculated (90,000 fragments/mL of water) at the base of the stem, and irrigation was performed to promote pathogen growth. The temperature oscillations in the greenhouse ranged from 22 to 28 °C and the relative humidity ranged from 45 to 100 % (Figure 1).

Once the first damage by P. capsici was observed in the pepper seedlings, the incidence of damage by treatment (isolates) was evaluated every 24 hours (when they reached 100 % damage) by using an ordinary scale from 0 (no damage) to 10 (necrotic tissue and dead plants), as previously described by Moran-Bañuelos et al. (2010). With the recorded readings, the incidence of damage was estimated using the following formula:

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Where li= incidence of diseased seedlings at moment i; ni= number of diseased seedlings at time i; and Ni= total population of inoculated seedlings. The days elapsed from the transplantation to the death of the seedlings were also evaluated once the first incidence of damage was observed; a weighted average for the damage was calculated and the cumulative damage was calculated based on the damage incidence scale (Moran-Bañuelos et al., 2010). A key variable was the disease progression through the area under the disease progress curve (AUDPC), which was based on the trapezoidal integration method, and it was determined using the following equation:

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Where n= number of evaluations; ti+1 = time of evaluation (d, days); ti = time of (d) immediate evaluation; y+1= damage severity (%) in ti; and yi = severity (%) in ti. In addition, the number of dead plants was quantified by evaluating the isolate and days elapsed from the inoculation to the death of the plants, and for descriptive purposes, the percentage of dead plants was calculated.

Statistical analysis

From the data calculated in the damage assessments generated for each treatment or each isolate and in each repetition, analyses of variances and comparisons of means were performed by the Tukey method (p<0.05) to determine the differences between the isolates and the control. The analyses were performed using SAS® version 9.0 statistical software.

Results and Discussion

Incidence of damage

The isolates obtained from diseased chili pepper plants in the Oaxaca Valley communities corresponded to P. capsici. The identification of the pathogen indicates that both the pathogen and the damages to the chili pepper crops in the Oaxaca Valley prevail, as previously documented by Vásquez et al. (2009) when they were studying the etiology of P. capsici in the same region. Lamour & Hausbeck (2002) noted that P. capsici is polycyclic; it can remain in the soil and produce sporangia that release spores, which are transported by wind or water. When the spores find adequate host and environmental conditions, the pathogen reproduces asexually or sexually, which bolsters the pathogen’s invasion of crops such as the chili pepper. Thus, the chili pepper producers of the Oaxaca Valley do not sow the same crop continuously in the same plots if P. capsica damage has been observed during a crop cycle.

An evaluation of the incidence of damage caused by eight inocula and a control without inoculation showed significant differences (p≤0.01) between the origins of the inocula and the average damage, cumulative damage, days to seedling death and area under the disease progression curve (Table 2). The differences in the damage among origins of the inocula indicate that each isolate evaluated here has differences in the invasion and the death of cells, organs and seedlings, perhaps due to the aggressiveness or segregation of cell wall-degrading pectins (Feng et al., 2010).

Table 2.

Significance of square means in the analysis of variances of variables indicators of damage caused by inoculations of Phytophthora capsici to seedlings of ‘costeño’ pepper.


Sources of variation df Weighted average
of damage
Cumulative
damage
Days to death
of seedlings
AUDPC1
Replications (R) 2 2.3ns 9.2ns 0.26ns 70.6ns
Inoculums 7 71.2** 106.9** 20.82** 3631.7**
Seedlings/R 33 1.6ns 21.3ns 0.55ns 97.3ns
Error 23 2.02 21.8 0.56 110.3
Variation coef. (%) 6 27.2 26.3 20.2 30.1

TFN1df= degree of freedom; nsnot significant (p>0.05); **significant at p≤0.01. 1AUDPC= Area under disease progress curve.


The seedling symptoms began with yellowing of the lower leaves, then the presence of gray to dark spots on the stem, the shedding of lower leaves, the onset of leaf wilt and stem collapse, and stem necrosis and seedling death (5 days). These are the characteristic symptoms of Capsicum spp. as indicated by Velásquez-Valle et al. (2001). The weighted average of the damages is an indicator of the percentage of seedling mortality through the evaluated experimental units. In this case, the isolates from San Jose del Progreso, Villa de Etla and San Antonino Castillo Velasco showed more than 40 % damage relative to the total seedlings as evaluated by isolate (Table 3).

Table 3.

Comparison of means of damage incidence by eight isolate de P. capsici on seedlings of ‘costeño’


Origin of isolates from Oaxaca, Mexico Weighted average of damage Cumulative damage Days to death of seedlings AUDPC1 (%)
San José El Progreso 47.1 a2 390.8 ab 8.7 e 2056.3 a
Ocotlán de Morelos 15.9 d 347.2 abc 23.8 a 544.5 d
Magdalena Teitipac 27.3 b 343.1 abc 13.9 cd 1509.4 b
San Jerónimo Tlacochahuaya 17.0 cd 283.7 bc 20.4 ab 810.1 cd
Villa de Etla 43.2 a 415.6 a 10.2 de 1958.3 a
San Juan de Dios Etla 17.9 bcd 251.6 c 19.9 ab 838.3 cd
San A. Castillo Velasco, San Jerónimo Taviche 50.0 a 365.6 abc 7.5 e 2160.6 a
El Carrizal, Cuilapam 26.4 bc 299.4 abc 16.6 bc 1235.6 bc
Testigo sin inoculaciones WVD3 WVD WVD WVD

TFN21AUDPC = Area under disease progress curve, on base to Moran-Bañuelos et al. (2010); 2in column, means with letter are not different significantly (Tukey’s test, p<0.05); 3WVD = without visual damage.


The results showed that once P. capsici invades the seedling, it causes seedling death in less than 25 days. However, the most aggressive isolates were those collected in San Jose del Progreso, San Antonino Castillo Velasco, and Villa de Etla and Magdalena Teitipac, which cause seedling death in 7.5 to 14 days (Table 3). Although the pathogenic races were not identified, we can infer that each inoculum has the capacity to invade the intercellular spaces or break the cell walls in the roots, stems, and leaves and cause the deaths of chili pepper seedlings.

Regarding the area under the disease progress curve (AUDPC), previous observations regarding the incidence of the disease were confirmed. The inocula obtained in San José del Progreso, Villa de Etla and San Antonino Castillo Velasco showed greater areas under the curve and significant differences in the areas estimated for the inoculants from Ocotlán, San Jerónimo Tlacochahuaya and San Juan de Dios Etla (Table 3). The variation in AUDPC values had a significant negative correlation (r=-0.97) with the days elapsed from inoculation to seedling death. The larger the AUDPC, the shorter the time was leading to seedling death, which suggests different pathogenicity among isolates.

The results for the incidence of damage caused by different isolates from different communities show that the ‘costeño’ pepper population was susceptible to P. capsici. Therefore, ‘costeño’ pepper is not a source of germplasm for P. capsica resistance. Thus, only isolates with a higher degree of pathogenicity should be evaluated to identify P. capsica tolerance or possible resistance among populations or accessions of chili peppers.

Incidence of damage by Rhizoctonia solani

The first detection of damage occurred five days after inoculation, and from that day on, the recording of the damage incidence in the ‘costeño’ pepper plants began. In the analysis of variance, there were no significant differences (p<0.05) between the isolates in relation to the area under the disease progress curve (AUDPC), the plant damage and the days to the deaths of the plants (Table 4).

Table 4.

Significance of square means of the analysis or variances of variables related with damage incidence by two isolations of R. solani on seedlings of ‘costeño’ pepper.


Sources of variation df1 AUDPC2 Damage per plant Days to seedling deaths
Replications (R) 2 4.0 x 10-5 ns 0.09ns 0.53ns
Isolations 1 9.0 x 10-5 ns 0.76ns 0.29ns
Seedlings/R 33 6.9 x 10-5 ns 0.14ns --
Error 31 10.5 x 10-5 0.23 0.37
Variation coef. (%) 54.9 27.6 21.9

TFN31df = degree of freedom; 2AUDPC = Area under disease progress curve; nsnot significant (p>0.05).


In the comparison of the damage effect caused by inoculations of R. solani in ‘costeño’ pepper seedlings, significant differences were observed with respect to the control. In this case, the control did not exhibit damage, unlike the inoculated treatments, thereby confirming that the presence of R. solani causes severe damage to the seedlings and is a relevant pathogen in the complex that induces pepper wilt as reported by Velásquez-Valle et al. (2001) and Vásquez et al. (2009). Among the isolates evaluated here, no significant differences were detected (p>0.05) for all the evaluated variables, including the number of days to diseased seedling death and the mortality percentage, but they differed significantly with respect to the control (Table 5).

Table 5.

Comparison of means of damage incidence by inoculations of two isolates from R. solani, on seedlings of ‘costeño’ pepper.


Isolates of R. solani AUDPC1 Damage per plant (%) Days to seedling deaths Mortality (%)
Isolate 1 722.0 a2 55.4 a 8.2 a 38.9
Isolate 2 443.9 a 39.4 a 9.2 a 33.3
Control without inoculum WVD3 WVD 0.0 0.0

TFN41AUDPC = Area under disease progress curve; 2means with same letter are not different significantly (Tukey’s test, p< 0.05); 3WVD = without visible damage.


The absence of significant differences in all the variables evaluated between the inoculations of the isolates does not indicate the absence of damage (Pérez-Acevedo et al., 2017). The evidence of damage is observed in the area under the disease progress curve from 443.9 to 722.0 units, with the damage percentages per plant ranging from 39.9 to 55.4 %. In this study, once the seedlings showed increasing damage progress, death occurred from 8.2 to 9.2 days on average, and there was a mortality of 33.3 to 38.9 %. This result suggests that the R. solani isolates evaluated here were virulent in ‘costeño’ pepper seedlings and can cause important economic losses by affecting plants that initially grew and produced crops.

In the field, high soil humidity, high relative humidity, cloudy days and high temperatures favor the presence of R. solani, thereby resulting in the damping off of seedlings (González-Perez et al., 2004), and when combined with Phytophthora capsici, it leads to chili pepper wilt. In this experiment, the results show that the conditions in which the experiment was performed also favored the presence of R. solani, and therefore, it is possible to conduct experimental evaluations of chili pepper populations to detect possible sources of tolerance or resistance to this pathogen.

Cubeta & Vilgalys (1997) and Muhyi & Bosland (1995) argue that it is pertinent to evaluate the R. solani tolerance or resistance of new genetic stocks or new improved varieties using inoculations of the pathogen with different geographical origins for the isolates. This approach is suggested because it is not sufficiently ethical to declare a population or variety of chili pepper ‘resistant’ unless it has been evaluated against a broad sample of genetic variability from virulent sources of R. solani and P. capsici. That is, susceptible populations must be rigorously separated from tolerant or resistant populations or varieties.

Conclusions

The isolates of P. capsici with greater pathogenicity were those from San José del Progreso and San Antonino Castillo Velasco, and they may be useful for identifying possible sources of tolerance to P. capsici. The average damage by R. solani in ‘costeño’ pepper seedlings was greater than 40 %, which indicates that both evaluated isolates are pathogenic. The population of ‘costeño’ pepper used in this study was susceptible to both pathogens.


fn1Cite this paper: Gómez-Hernández, D.; Carrillo-Rodríguez, J. C.; Chávez-Servia, J. L.; Perales-Segovia, C. (2018). Pathogenicity of Phytophthora capsici Leon and Rhizoctonia solani Khün, on seedlings of ‘costeño’ pepper (Capsicum annuum L.). Revista Bio Ciencias 5, e356. doi: https://doi.org/10.15741/revbio.05.e356

References
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Revista Bio Ciencias, Año 13, vol. 9,  Enero 2022. Sistema de Publicación Continua editada por la Universidad Autónoma de Nayarit. Ciudad de la Cultura “Amado Nervo”,  Col. Centro,  C.P.: 63000, Tepic, Nayarit, México. Teléfono: (01) 311 211 8800, ext. 8922. E-mail: revistabiociencias@gmail.com, revistabiociencias@yahoo.com.mx, http://revistabiociencias.uan.mx. Editor responsable: Dra. Karina J. G. Díaz Resendiz. No. de Reserva de derechos al uso exclusivo 04-2010-101509412600-203, ISSN 2007-3380, ambos otorgados por el Instituto Nacional de Derechos de Autor. Responsable de la última actualización de este número Dra. Karina J. G. Díaz Resendiz Secretaria de Investigación y Posgrado, edificio Centro Multidisciplinario de Investigación Científica (CEMIC) 03 de la Universidad Autónoma de Nayarit. La opinión expresada en los artículos firmados es responsabilidad del autor. Se autoriza la reproducción total o parcial de los contenidos e imágenes, siempre y cuando se cite la fuente y no sea con fines de lucro.

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Revista Bio Ciencias por Universidad Autónoma de Nayarit se encuentra bajo una licencia de Creative Commons Reconocimiento-NoComercial-SinObraDerivada 4.0 Internacional

Fecha de última actualización 9 de Junio de 2022

 

licencia de Creative Commons Reconocimiento-NoComercial-SinObraDerivada 4.0 Internacional

 

Dra. Karina J. G. Díaz Resendiz