Leaves arise from the flank of the shoot apical meristem and are asymmetrical along the adaxial/abaxial plane from inception. Mutations perturbing dorsiventral cell fate acquisition in a variety of species can result in unifacial (radially symmetrical) leaves lacking adaxial/abaxial polarity. However, mutations in maize (Zea mays) ragged seedling2 (rgd2) condition cylindrical leaves that maintain dorsiventral polarity. Positional cloning reveals that rgd2 encodes an ARGONAUTE7 (AGO7)-like protein required to produce ta-siARF, a trans-acting small interfering RNA that targets abaxially located auxin response factor3a (arf3a) transcripts for degradation. Previous studies implicated ta-siARF in dorsiventral patterning of monocot leaves. Here, we show that arf3a transcripts hyperaccumulate but remain abaxialized in rgd2 mutant apices, revealing that ta-siARF function is not required for arf3a polarization. RGD2 also regulates miR390 accumulation and localization in maize shoot apices. Similar to the abaxialized maize mutant leafbladeless1 (lbl1), rgd2 mutants exhibit ectopic accumulation of the abaxial identity factor miR166 in adaxial domains. Thus, hyperaccumulation of arf3a and ectopic accumulation of miR166 are insufficient to condition abaxialized leaf phenotypes in maize. Finally, transcripts of a maize ago1 paralog overaccumulate in lbl1 but not in rgd2 mutants, suggesting that upregulation of ago1 combined with ectopic accumulation of miR166 contribute to abaxialized leaf formation in lbl1. We present a revised model for the role of small RNAs in dorsiventral patterning of maize leaves.
Objective: This study was undertaken to examine the effect of successive pregnancies over a 3-year
period on the course of maternal human immunodeficiency virus (HIV) infection and the rate of
perinatal transmission of HIV.
Methods: A retrospective analysis of 32 pregnancies in 14 known HIV-infected women vs. a
matched control group of HIV-infected women who had been pregnant only once was done.
Results: The multiple-pregnancy group was similar to the single-pregnancy group for age, race,
duration of known HIV infection, initial CD4 count, and date of first pregnancy. The delivery data
were similar as well. The CD4 counts in the multiple-pregnancy group fell from 595 to 460, while
counts in the single-pregnancy group fell comparably from 669 to 638, both over 37 months
(P = 0.1476). Five of 5 second-born infants of known serostatus vs. 8 of 21 first-born infants were
HIV-infected (P < 0.05).
Conclusions: Successive pregnancies do not alter the course of HIV infection in asymptomatic
women followed up to 3 years. The infants of second pregnancies of known HIV-infected women
may be at higher risk for perinatal transmission.
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