Much like PRD 4, both MUS 58 and MUS 59 were phosphorylated in reaction to MMS therapy. From these results, we concluded that the recently identified genes and prd 4 are involved in signal transduction after DNA damage. It’s interesting that both CHK2 homologues Lapatinib Tykerb get excited about DNA damage response in D. crassa as may be the case in S. cerevisiae. In S. cerevisiae, two genes that encodes structural associated proteins with CHK2 involve in DNA damage checkpoint, in other creatures, just one CHK2 homologue involved in this process has been noted, like, cds1 in S. pombe, mnk in D. melanogaster, and chk 2 in D. ele gans. But, the features of CHK2 homologues differ in D. crassa and S. cerevisiae. Both RAD53 and DUN1 are involved not just in DNA damage response but in addition in get a handle on of the creation of dNTPs through up regulation of ribonucleotide reductase. The null mutant of RAD53 is inviable because of hunger of nucleotides, and both RAD53 and DUN1mutants are very sensitive and painful to theRNRinhibitorHU. Nevertheless, themus 59 or prd 4 disruptant hotel. Any growth defect wasn’t shown by crassa, and HU sensitivities of the mus 59 and prd 4mutants Lymphatic system were indistinguishable fromthat of the wild type strain. These results suggest that mus 59 and prd 4 do not subscribe to the creation of dNTPs. To elucidate whether characteristics of mus 59 and prd 4 are repetitive, a 59 prd 4 doublemutant was built. HU sensitivity of the doublemutant was corresponding to that of the singlemutants, indicating these genes are actually dispensable for the dNTP creation. Because S. cerevisiae RAD53 and DUN1 are very important for responses to many kinds of DNA damage, theirmutants show higher sensitivities to UV, chemical mutagens and IR than those of the wild type strain. But, this aspect can be in disagreement with D. crassa CHK2 homologues. The mus 59 and the prd Hedgehog inhibitor 4 mutants were extremely sensitive and painful to CPT but showed behaviors similar to those of the wild type strain against other mutagens. These studies claim that the experience of the MUS 59 and PRD 4 kinases is required only in response to DNA strand breaks caused by CPT therapy. The mus 59 prd 4 doublemutant is also less vulnerable to mutagens with the exception of CPT. And the CPT awareness of the doublemutant was almost same level with that of the mus 59 mutant, indicating these genes concern a same route. On another hand, increased sensitivity of the mus58 mutant and MUS 58 phosphorylation was observed in reaction to many kinds of mutagens and HU therapy, suggesting the MUS 58 kinase is involved in the key signalling pathway, which are induced by many kinds of DNA damage and replication fork arrest in D. crassa.