High impact information on mr

• In dividing cells mr mutations cause a metaphase arrest, and endo cycling nurse cells inappropriately reenter mitosis in mr mutants [1].
• The mr mutants further indicate that transient mitotic functions in endo cycles change chromosome morphology from polytene to polyploid [1].
• We show mr encodes the APC2 subunit of the anaphase promoting complex/cyclosome [1].
• Oct-4 may also regulate the molecular differentiation of cells in the germ lineage as it progresses from the fertilized egg, through cleavage stage/morula blastomeres, blastocyst, inner cell mass, epiblast, germ cells, and gametes [2].
• Embryonic S-M cycles and the archetypal (G1-S-G2-M) cell cycle are both arrested in metaphase in different morula mutants [3].

Biological context of mr

• In the embryo, the expression of XBMP-1 increased gradually from the morula to the swimming tadpole stages [4].

Other interactions of mr

• Consistent with this, we found cyclin B protein to be inappropriately present in morula mutant nurse cells [3].
• Thus morula serves a dual function as a cell cycle regulator that promotes exit from mitosis and maintains the absence of mitosis during the endo cycle, possibly by activating the cyclin destruction machinery [3].

Analytical, diagnostic and therapeutic context of mr

• Northern blotting revealed that the mRNA for HpCycE is maintained at a high level up to the morula stage and thereafter declines [5].

References