natural spread
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2021 ◽  
Author(s):  
Judith K Brown

Abstract Cotton leaf curl Gezira virus (CLCuGV) is endemic to the African Sahel region (Idris et al., 2000). It is an economically important cotton-infecting begomovirus, and poses a serious threat to cotton production. It causes yield loss in all affected cotton-growing areas in Africa. Losses are difficult to assess, but estimates range up to 20% when infection occurs early in the growing season and/or with highly susceptible cultivars. Natural spread is mainly by the whitefly vector, Bemisia tabaci, which transmits the virus in a persistent, circulative manner. Viruliferous whiteflies on infested/infected plants harbouring CLCuGV imported to other countries are of concern for preventing introduction.


2021 ◽  
Author(s):  
John Randles ◽  
Judith Rodriguez ◽  
Ganesan Vadamalai ◽  
Dagmar Hanold ◽  
Lalith Perera

Abstract Cadang-cadang disease (caused by Coconut cadang-cadang viroid; CCCVd) is widely distributed in the central Philippines. It continues to spread at high rates in some provinces within the disease zone whereas other sites do not show increases in incidence. New outbreaks have been reported outside earlier boundaries of distribution. Incidence is negligible in plantations less than 10 years old, but increase is then linear at various rates up to ~1% pa. No vector has been implicated in spread so the mode of natural spread is unknown. Variants of CCCVd occur in other members of the Arecaceae including oil palm and buri palm and viroid-like sequences related to CCCVd have also been identified in a range of tropical monocotyledons in South-East Asia and Oceania. However, diagnostic facilities are poorly represented where the disease and viroid occur, and epidemiology is incompletely researched.


2021 ◽  
Author(s):  

Abstract The European larch canker pathogen, L. willkommii, is apparently native to Japan, but established in Europe, where it became well known due to its damage to plantations of exotic and native Larix species, beginning in the nineteenth century. It attacks and spreads among the various species of Larix once it has been introduced. It was detected as an invasive to North America on two occasions; once in the northeastern USA in the 1920s (Hahn and Ayres, 1936) and once in the eastern maritime provinces of Canada in the 1980s (Magasi and Pond, 1982). Efforts to prevent its introduction across natural barriers include regulation and restriction of trade and transport of susceptible species and bark-bearing products made from them. Control by destruction of infected plants or plant parts is often made difficult by the size of the trees concerned (Tegethoff, 1965). Local spread of the fungus between trees appears to depend on dissemination and survival of airborne ascospores. Climatic conditions of humidity and temperature appear to limit natural spread from regions of establishment (Ostaff, 1985).


Author(s):  
Aydin Uzun ◽  
Ayşe Çil ◽  
Mehmet Yaman ◽  
Ömer Faruk Coşkun

Turkey with diverse ecologies harbours several plant and fruit species. Several species grow naturally are grown commercially. Kayseri and surroundings constitute natural spread zone of some fruit species. This study was conducted to determine genetic diversity and some pomological characteristics of 31 seed-propagated quince (Cydonia oblanga Mill.) genotypes. For pomological characteristics, fruit length, fruit width, water soluble dry matter (WSDM) and total acidity analyses were performed. Molecular analyses were conducted with the aid of 15 SRAP primer combinations. Genetic diversity in investigated genotypes varied between 0.53- 0.92 and genotypes were gathered under two main groups. Primer base lengths varied between 400- 1700 bp. A total of 97 clear bands were obtained and 91 of them were polymorphic (polymorphism ratio = 87.7%). Present findings revealed that existing quince populations of the region should be preserved and be used in further genetic studies.


2019 ◽  
Vol 35 (1) ◽  
pp. 58-69 ◽  
Author(s):  
Mike R Wilson ◽  
Jeanne Holladay ◽  
Ronald L Chandler

Abstract STUDY QUESTION Is it possible to establish a genetically engineered mouse model (GEMM) of endometriosis that mimics the natural spread of invasive endometrium? SUMMARY ANSWER Endometriosis occurs in an ARID1A (AT-rich interactive domain-containing protein 1A) and PIK3CA (phosphatidylinositol-4,5-bisphosphate 3-kinase, catalytic subunit alpha) mutant GEMM of endometrial dysfunction following salpingectomy. WHAT IS KNOWN ALREADY Although mouse models of endometriosis have long been established, most models rely on intraperitoneal injection of uterine fragments, steroid hormone treatments or the use of immune-compromised mice. STUDY DESIGN, SIZE, DURATION Mice harboring the lactotransferrin-Cre (LtfCre0/+), Arid1afl, (Gt)R26Pik3ca*H1047R and (Gt)R26mTmG alleles were subject to unilateral salpingectomies at 6 weeks of age. Control (n = 9), LtfCre0/+; (Gt)R26Pik3ca*H1047R; Arid1afl/+ (n = 8) and LtfCre0/+; (Gt)R26Pik3ca*H1047R; Arid1afl/fl (n = 9) were used for the study. The (Gt)R26mTmG allele was used for the purpose of fluorescent lineage tracing of endometrial epithelium. LtfCre0/+; (Gt)R26mTmG (n = 3) and LtfCre0/+; (Gt)R26Pik3ca*H1047R/mTmG; Arid1afl/fl (n = 4) were used for this purpose. Mice were followed until the endpoint of vaginal bleeding at an average time of 17 weeks of age. PARTICIPANTS/MATERIALS, SETTING, METHODS At 6 weeks of age, mice were subjected to salpingectomy surgery. Mice were followed until the time point of vaginal bleeding (average 17 weeks), or aged for 1 year in the case of control mice. At time of sacrifice, endometriotic lesions, ovaries and uterus were collected for the purpose of histochemical and immunohistochemical analyses. Samples were analyzed for markers of the endometriotic tissue and other relevant biomarkers. MAIN RESULTS AND THE ROLE OF CHANCE Following salpingectomy, LtfCre0/+; (Gt)R26Pik3ca*H1047R/mTmG; Arid1afl/fl mice developed endometriotic lesions, including lesions on the ovary, omentum and abdominal wall. Epithelial glands within lesions were negative for ARID1A and positive for phospho-S6 staining, indicating ARID1A-PIK3CA co-mutation status, and expressed EGFP (enhanced green fluorescent protein), indicating endometrial origins. LARGE-SCALE DATA N/A LIMITATIONS, REASONS FOR CAUTION LtfCre0/+; (Gt)R26Pik3ca*H1047R; Arid1afl/fl mice develop vaginal bleeding as a result of endometrial dysfunction at an average age of 17 weeks and must be sacrificed. Furthermore, while this model mimics the natural spread of endometriotic tissue directly from the uterus to the peritoneum, the data presented do not reject current hypotheses on endometriosis pathogenesis. WIDER IMPLICATIONS OF THE FINDINGS The idea that endometriosis is the result of abnormal endometrial tissue colonizing the peritoneum via retrograde menstruation has gained widespread support over the past century. However, most models of endometriosis take for granted this possibility, relying on the surgical removal of bulk uterine tissue and subsequent transplantation into the peritoneum. Growing evidence suggests that somatic mutations in ARID1A and PIK3CA are present in the endometrial epithelium. The establishment of a GEMM which mimics the natural spread of endometrium and subsequent lesion formation supports the hypothesis that endometriosis is derived from mutant endometrial epithelium with invasive properties. STUDY FUNDING/COMPETING INTEREST(S) This research was supported by the American Cancer Society PF-17-163-02-DDC (M.R.W.), the Mary Kay Foundation 026-16 (R.L.C.) and the Ovarian Cancer Research Fund Alliance 457446 (R.L.C.). The authors declare no competing interests.


PLoS ONE ◽  
2015 ◽  
Vol 10 (7) ◽  
pp. e0134126 ◽  
Author(s):  
Julien Haran ◽  
Alain Roques ◽  
Alexis Bernard ◽  
Christelle Robinet ◽  
Géraldine Roux

2015 ◽  
Vol 10 (2) ◽  
pp. 63-73 ◽  
Author(s):  
Bodrun Nessa ◽  
Moin U. Salam ◽  
A.H.M. Mahfuzul Haque ◽  
Jiban K. Biswas ◽  
M. Shahjahan Kabir ◽  
...  

2014 ◽  
Vol 163 (5) ◽  
pp. 395-406 ◽  
Author(s):  
Shailender Kumar ◽  
Prachi Sharma ◽  
Susheel Sharma ◽  
G. P. Rao

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