An obvious possibility is the design of alternative management methods for the control of this pest species, such as sterile insect techniques and/or insertion of fitness reduction factors aiming at pest suppression or replacement. These endosymbionts may prove important in strain divergence, with implications for grain loss and weevil control because endosymbiont load and cooccurrence affect grain consumption, consequently affecting grain loss and leading to higher economic losses. In addition, both endosymbiont load and co-occurrence affect insect activity, interfering with their dispersal and colonization, producing added potential consequences for pest control, which is variable between populations and even among individuals in a population. Other unforeseeable consequences may also derive from variable endosymbiont loads and co-occurrence in arthropod pest species in general, and grain weevils in particular, which is likely to draw further attention in the future. Vertebrate eye formation is contingent on the complex interactions of transcription factors that regulate the expression of target genes. The precise temporal regulation of these genes is essential for normal eye development. Mutations in the genes encoding these transcription factors lead to severe congenital eye defects such as anophthalmia, aphakia and microphthalmia. These severe ocular diseases are found in approximately 30 of every 100,000 blind children worldwide. However, the precise pathogenesis and the optimal treatment protocols remain unclear. To date, several mutations in genes that mediate ocular development have been identified in humans. To VE-822 1232416-25-9 identify crucial genes and modifier genes that regulate ocular development and disorders, the establishment of mouse models may be highly effective. Specifically, profound ocular diseases are genetically heterogeneous, with potentially overlapping phenotypes resulting from mutations in multiple genes and varying phenotypes caused by different mutations in a single gene. Additionally, anophthalmia and microphthalmia show some evidence of familial recurrence but usually no clear Mendelian transmission pattern, which may be a reflection of several potentially interactive factors such as oligogenic causation, geneenvironment interactions, and stochastic variations in development. Therefore, mouse models that have allelic variants and varied genetic backgrounds in Pitx3 will provide essential information for understanding the mechanisms of ocular pathogenesis and development. This previous study revealed that the PITX3 p.Gly220ProfsX94 mutation results in a partial loss of function and does not have a dominant negative effect. The p.Gly220ProfsX94 mutation located in the distal region of the homeodomain has been found in multiple pedigrees and causes dominant cataracts often accompanied by severe ASMD.