Furthermore, the male germline accumulates more DNA replication errors because of the higher number of germline cell divisions in males than females. Therefore, PHEX mutagenesis in paternal germ cells is likely more frequent in sporadic patients and would only affect the female offspring, which is accordance with our finding from family 9. Interestingly, however, that the 2 sporadic patients in our study are males, which differs from the demographics in previous studies. This finding indicates that the mutated PHEX alleles in sporadic male patients probably resulted from the mutagenesis in the X chromosome of the maternal germ cell. From our study, there are no significant differences of gene mutation types and mutation locations in the PHEX gene in Chinese XLH patients compare to non-Chinese patients. However, the same mutations in different races can cause different clinical features. For example, p.Trp444X was firstly reported by Beck-Nielsen SS, et al. in a sporadic patient, a Danish male, with a normal height, mild Dobutamine hydrochloride skeletal and endodontic phenotype. Whereas, in our study, the mutation was found in familial patients with abnormal gait, kyphosis, and hip and knee joint pain. In addition, we identified that the proband and her daughter carried the non-sense mutation which consisted of a heterozygous G to A transition at c.1332 in exon 12, while, The mutation reported by Beck-Nielsen SS, et al. is c.1331G.A affecting one nucleotide upstream the one described in our manuscript. Although, the result is the same at the protein level with a tryptophan at position 444 being substituted by a stop codon and truncation at p. 444, the clinical features are quite different in Chinese patients compare to non-Chinese patients. Although, no evident genotype phenotype correlation could be established in our study, 2 novel mutations were detected and different clinical features were described. Therefore, Functional studies investigating the PHEX gene mutation should be performed to elucidate the complex relationship between genotype and phenotype. Seed germination, a key ecological and agronomic trait for seed plants, determines when plants enter natural or agricultural ecosystems and marks the beginning of a new Dilazep dihydrochloride growth cycle. It is controlled by both intrinsic and environmental cues, which are mainly regulated by two antagonistic phytohormones, abscisic acid and gibberellin. ABA is a negative regulator of seed germination, while GA promotes the completion of germination, counteracting the effects of ABA.