Establishment of the Invasive Cactus Moth, \u3ci\u3eCactoblastis cactorum\u3c/i\u3e (Berg) (Lepidoptera: Pyralidae) in Pakistan: A Potential Threat to Cultivated, Ornamental and Wild \u3ci\u3eOpuntia\u3c/i\u3e spp. (Cactaceae)

Subsequent to the significant accomplishment of biological control of Opuntia weeds in Australia, the larvae of the cactus moth, Cactoblastis cactorum (native to parts of South America), were released in many countries for the biological control of native Opuntia species (Simmonds and Bennett, 1966). Inauspiciously, larvae were also released in the Caribbean, where the moth spread naturally and by the human support all over the region (García-Turudi et al., 1971). Its enhanced dissemination rate and the biological potential for invasiveness, suggests that the cactus moth is likely to become an invasive pest of Opuntia in the Southeast United States, Mexico, and southwestern America. Its damage is restricted mainly to the plants of genus Opuntia (plants with the characteristic of flat prickly pear pads of the former genus Platyopuntia, now considered to be the part of the genus Opuntia). In this region, plants of this genus provide valuable resources for humans, livestock, and wildlife such as food, medicine, and emergency fodder, while in the arid and semi-arid regions, the plants play key roles in ecosystem processes and soil conservation. At present, the cactus moth has developed into a severe threat to the high diversity of prickly pear cacti, all over the world for both the native and cultivated species of Opuntia (IAEA, 2002)

Deleterious Variants in WNT10A, EDAR, and EDA Causing Isolated and Syndromic Tooth Agenesis: A Structural Perspective from Molecular Dynamics Simulations

The dental abnormalities are the typical features of many ectodermal dysplasias along with congenital malformations of nails, skin, hair, and sweat glands. However, several reports of non-syndromic/isolated tooth agenesis have also been found in the literature. The characteristic features of hypohidrotic ectodermal dysplasia (HED) comprise of hypodontia/oligodontia, along with hypohidrosis/anhidrosis, and hypotrichosis. Pathogenic variants in EDA, EDAR, EDARADD, and TRAF6, cause the phenotypic expression of HED. Genetic alterations in EDA and WNT10A cause particularly non-syndromic/isolated oligodontia. In the current project, we recruited 57 patients of 17 genetic pedigrees (A-Q) from different geographic regions of the world, including Pakistan, Egypt, Saudi Arabia, and Syria. The molecular investigation of different syndromic and non-syndromic dental conditions, including hypodontia, oligodontia, generalized odontodysplasia, and dental crowding was carried out by using exome and Sanger sequencing. We have identified a novel missense variant (c.311G>A; p.Arg104His) in WNT10A in three oligodontia patients of family A, two novel sequence variants (c.207delinsTT, p.Gly70Trpfs*25 and c.1300T>G; p.Try434Gly) in EDAR in three patients of family B and four patients of family C, respectively. To better understand the structural and functional consequences of missense variants in WNT10A and EDAR on the stability of the proteins, we have performed extensive molecular dynamic (MD) simulations. We have also identified three previously reported pathogenic variants (c.1076T>C; p.Met359Thr), (c.1133C>T; p.Thr378Met) and (c.594_595insC; Gly201Argfs*39) in EDA in family D (four patients), E (two patients) and F (one patient), correspondingly. Presently, our data explain the genetic cause of 18 syndromic and non-syndromic tooth agenesis patients in six autosomal recessive and X-linked pedigrees (A-F), which expand the mutational spectrum of these unique clinical manifestations.status: publishe