Therefore, the seam cell defects observed in mdf 2 young adult worms could be either due to defective embryonic cell divisions, or alternatively, defective postembryonic divisions. In order to address these two possibilities, we scored the number of seam cell nuclei in newly hatched www.selleckchem.com/products/Vandetanib.html wild type and mdf 2 L1 larvae. The wild type animals analyzed had an average number of 10. 02 SCM,GFP nuclei per side. Similarly, the majority of the mdf 2 newly hatched larvae had 10 SCM,GFP positive nuclei with 9. 75 average and 8 11 range. Although, unpaired students t test analysis revealed a significant difference, both the quantitative and qualitative defects observed in mdf 2 newly hatched larvae were much less severe than defects observed in L4 or adults.

Therefore, we conclude that MDF 2 plays an important role in post embryonic seam cell development. Recently, it was reported that MDF 1 plays an impor tant role in nutrient deprivation induced somatic cell arrest. Namely, it was found that hemizygosity of mdf 1 causes an increase in seam cell numbers from 10, observed in wild type L1 worms starved for four days, to between 12 and 17 in more than half of the mdf 1 L1 worms. To analyze the ability of mdf 2 hemizygotes to arrest the proliferation during L1 diapause, we starved wild type and mdf 2 hatchl ings for four days. Subsequent analysis of the seam cells revealed that neither wild type nor mdf 2 larvae had more than 11 SCM,GFP positive nuclei, indicating starvation induced L1 larval arrest. Thus, unlike MDF 1, MDF 2 component of the SAC does not seem to be required for starvation induced somatic cell cycle arrest.

The seam cell defect of mdf 2 is due to defects in the proliferative seam cell division The seam cells have stem cell like properties and divide four times in developing larva for self renewal maintenance, expansion, and to produce differentiated cells. Six out of 10 embryonic seam cells, H1, V1 V4 and V6, undergo self renewal expansion division at L2, resulting in an increase in the number of seam cells to 16. To determine if the seam cell defect observed in mdf 2 homozygotes is due to a defect in proliferative cell division, we determined the number of SCM,GFP positive nuclei at late L2 and L3. We observed a mean of 14. 36 seam cell nuclei at late L2 in the mdf 2 homozygotes and a mean of 14.

08 seam cell nuclei at L3 in the mdf 2 homozygotes, which is not significantly different from the number of SCM,GFP nuclei observed in later stages of the mdf 2 homozy gotes. These data demonstrate that the seam cell defect observed in mdf 2 homozygotes is most likely due to cell division defects at Cilengitide L2. We next examined whether reduction of seam cell number could be attributed to failure of cell cycle pro gression of specific seam cells. We counted how often the observed seam cell defect is a consequence of failure of cell cycle progression of one particular cell.