To study the mechanism of potassium （K） application on improvement of maize resistance to stalk rot at cellular level, scanning electron microscope and transmission electron microscope were used to observe the effect of K on the ultrastructure of maize stalk pith tissue and young root tip cell influenced by K and pathogen. In K deficient treatment, parenchyma cells of stalk pith had abnormal structure, and the cell wall between upper and lower adjacent cell was damaged, resulting in the loss of connections between vascular cells and insufficient supporting capacity. However, an improved K nutrition helped to keep a quite tight arrangement of root cell with thick cell wall, and prevent the invasion of pathogen effectively. Moreover, K treated root cell had abundant golgi apparatus, which could excrete large amount of secretions to degrade mycelium. Papillary and highly electronic intensity dot were accumulated at the invading point to prevent the deveJopment of the mycelium. Improved K nutrition could increase the resistant ability of maize plant to stalk rot, through keeping cell structure stability, preventing the expansion of intracellular space to reduce the chances of pathogen invasions, and through reinforcing cell wall and formation of intercellular and intracellular material to restrict further development of pathogen in host cell.
Background X-linked hearing impairment is clinically and genetically a heterogeneous disease. Although many disorders manifest with hearing loss, a limited number of sex-linked loci and only one gene （POU3F4） have been shown to be implicated in X-linked non-syndromic hearing impairment. In the present study, we have performed a clinical and genetic analysis of a Chinese family with X-linked non-syndromic hearing loss, with emphasis on audiological findings and genomic mapping. Methods The clinical features of Family JX01 were evaluated by physical and audiometric examination in eighteen family members. Mutation screening of POU3F4 was identified by polymerase chain reaction （PCR） amplification and sequencing. Molecular evaluation consisted of X-chromosome wide genotyping by microsatellite makers （STR）, followed by analyzing using MLINK computer program. Results Five affected males demonstrated bilateral, symmetrical sensorineural and profound hearing loss. The hearing impairment started prelingual. The female carriers did not have any complain of hearing loss, however, two of them were tested with milder loss with high frequency. No causative mutations in POU3F4 gene were detected by DNA sequencing. Linkage analysis indicated that the responsible gene was linked to locus DXS1227 （maximum Iod score=2.04 at θ=0）. Conclusions The affected males in Family JX01 have profound prelingual sensorineural hearing impairment. In addition, two female carriers showed mild to moderate hearing losses. However, none of females complained of any hearing loss. Analysis of hereditary deafness in this family mapped most compatibly to the Xq27.2.
We present the clinical and genetic findings for a Chinese family with X-linked non-syndromic hearing loss in which the affected males showed congenital profound sensorineural hearing impairment. In two affected brothers, the computer tomography of temporal bone showed bilateral dilation of the internal auditory canal with fistulous communication between the lateral canal and the basal cochlear turn, which is consistent with the typical DFNX2 phenotype. A missense mutation （c.647G→A） in the POU3F4 gene caused a substitu- tion from glycine to glutamic acid at position 216 （p.G216E）, and this mutation was found to consistently cosegregate with the deafness phenotype in the family. The mutation resulted in the loss of function of the POU3F4 by decreasing the affinity between the protein and DNA, as shown in silico by the structural analysis. Prenatal diagnosis of pregnant proband of this family revealed the c.647G→A mutation in DNA extracted from the amniotic fluid surrounding the fetus. The appropriate use of genetic testing and prenatal diagnosis plays a key role in reducing the recurrence of genetic defects in high-risk families.
