Meiotic recombination 11
However recombination can be restored to near normal levels by a deletion in rad2 , a gene that encodes an endonuclease involved in Okazaki fragment processing Farah et al.
Both crossover and non-crossover recombination were increased but double-strand breaks were undetectable. On the basis of the biochemical properties of the rad2 deletion, it was proposed that meiotic recombination can be initiated by DNA lesions other than double-strand breaks, such as nicks and gaps which accumulate during premeiotic DNA replication when Okasaki fragment processing is deficient. The above findings indicate that DNA damages arising from a variety of sources can be repaired by meiotic recombination and that such a process can occur independently of SPO The most recent common ancestor of the social amoeba genera Dictyostelium , Polysphondylium and Acytostelium , appears to have lacked the Spo11 gene.
Bloomfield [7] speculated that dormant cells in the soil might be exposed to many kinds of stress, such as desiccation or radiation, that could induce spontaneous DNA damage. Such damage would make the induction of double-strand breaks by Spo11 redundant for the initiation of recombination during meiosis, and thus explain its absence in this group. From Wikipedia, the free encyclopedia.
Absence of Spo11 in some sexual species [ edit ] The most recent common ancestor of the social amoeba genera Dictyostelium , Polysphondylium and Acytostelium , appears to have lacked the Spo11 gene.
Jones and Bartlett Publishers, Inc. Retrieved from " https: Views Read Edit View history. This page was last edited on 1 March , at Homozygosity for null alleles is thought to be lethal in embryogenesis, as is the case in Mre11 knockout mice. Germline mutations have also been found in sporadic hematopoetic malignancies, with loss of the wild-type allele in the malignant cells. Somatic Rare mutations have been found in breast cancer and lymphoma.
In colon cancers not expressing Mre11, the mutation of a poly-T tract in intron 4 has been shown to induce a splicing error that truncates the protein.
Seven of 20 gastric tumors failed to express Mre11, although the cause of this was not demonstrated. The two disorders cannot be distinguished by their phenotypes, though there is some indication that ATLD may have a milder course. The severity of the disease may be dependent on the residual activity of the mutated Mre11 alleles.
Prognosis Poor, though the course of the disease may be milder than found in classic A-T. Bibliography Mre11 protein complex prevents double-strand break accumulation during chromosomal DNA replication.
InterPro P Splice isoforms: Mon May 14 Two isoforms are expressed, isoform 1 at nt; isoform 2, nt, transcribed from an alternative first noncoding exon and lacking exon 5.
Both isoforms are approximately 80 kDa. Mre11 participates in the repair of DNA double-strand breaks and replication errors as well as in meiotic homologous recombination. The hypomorphic argter, asnser and argter alleles have been described in ATLD patients. Rare mutations have been found in breast cancer and lymphoma. Ataxia telangiectasia - like disorder ATLD. Ataxia telangiectasia-like disorder is a progressive cerebellar degenerative disease with telangiectasia, immunodeficiency, cancer risk, radiosensitivity, and chromosomal instability.