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Then T has a unique fixed point in (Acap B).
Since A and B are closed in X, (omega in Acap B).
Then T has a unique fixed point in (Acap B). ([5], Theorem 2.12).
Then S and T have a point of coincidence in (Acap B).
Then (mathscr{U}) has a unique fixed point in (Acap B).
Thus by Corollary 2.12, T has the unique fixed point in (Acap B).
Similar(29)
Identification of the structural elements in ACAP-A/B responsible for the actin structural change and sporulation defect will test this hypothesis.
It is possible that domains other than ArfGAP present in GxcDD but not in ACAP-A/B might be crucial for streaming.
Since we observed abnormal actin structures in acap-A−/B− cells (Fig. 5B and C), we wondered if these defects would also lead to alterations in migration.
Consistent with the result of normal development on non-nutrient agar, exogenous cAMP pulsing induced timely expression of the early developmental markers, cAR1 and ACA in acap-A−/B− cells as in wild-type (Fig. 5A).
Therefore, although we did not observe any apparent spore shape change in acap-A−/B− cells, we can not exclude the possible role of ACAP-A and B in spore coat formation by regulating PSV formation and trafficking.
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