Since 3H4MV biosynthesis pathway has not yet been identified, these mutants might be useful in the study of this pathway.
These lucky mutants might be less likely to die of malaria, for example, or be better able to tolerate lactose or handle the complexities of full-blown language.
The "X-Men" mutants might be headed to your small screen, and not in cartoon form this time.
Lack of obvious meiotic phenotypes in GYRB3 mutants might be due to genetic redundancies.
Thus death of some mutants might be accompanied by faster degradation of chromosomal DNA than death of others.
If this specific isoform of MBD5 is also involved in this process, female Mbd5 mutants might be sterile.
Therefore, we speculated that at least some differentially activated AT1R mutants might be particularly prone to recruitment of β-arrestins.
This result also suggests that alterations in conidial surface of the color mutants might be a major factor responsible for the larvae darkening.
Based on the results described above, we suggested that the surface hydrophobicity defect of ΔpdeH and ΔpdeLΔpdeH mutants might be related to Mpg1 and Mhp1.
It is possible that defective centromere chromatin structures observed in mcl1 and swi7 mutants might be a secondary effect of an unstable DNA replication fork.
So we further tested whether these mutants might be also defective in the step that follows DNA binding, i.e., synapsis and DNA cleavage.
