The divergence between labeled training data and unlabeled testing data is a significant challenge for recent deep learning models. Unsupervised domain adaptation (UDA) attempts to solve such a problem. Recent works show that self-training is a powerful approach to UDA. However, existing methods have difficulty in balancing scalability and performance. In this paper, we propose an instance adaptive self-training framework for UDA on the task of semantic segmentation. To effectively improve the quality of pseudo-labels, we develop a novel pseudo-label generation strategy with an instance adaptive selector. Besides, we propose the region-guided regularization to smooth the pseudo-label region and sharpen the non-pseudo-label region. Our method is so concise and efficient that it is easy to be generalized to other unsupervised domain adaptation methods. Experiments on 'GTA5 to Cityscapes' and 'SYN-THIA to Cityscapes' demonstrate the superior performance of our approach compared with the state-of-the-art methods.
In mammals, the production of mature oocytes necessitates rigorous regulation of the discontinuous meiotic cell-cycle progression at both the transcriptional and post-transcriptional levels. However, the factors underlying this sophisticated but explicit process remain largely unclear. Here we characterize the function of N-acetyltransferase 10 (Nat10), a writer for N4-acetylcytidine (ac4C) on RNA molecules, in mouse oocyte development. We provide genetic evidence that Nat10 is essential for oocyte meiotic prophase I progression, oocyte growth and maturation by sculpting the maternal transcriptome through timely degradation of poly(A) tail mRNAs. This is achieved through the ac4C deposition on the key CCR4-NOT complex transcripts. Importantly, we devise a method for examining the poly(A) tail length (PAT), termed Hairpin Adaptor-poly(A) tail length (HA-PAT), which outperforms conventional methods in terms of cost, sensitivity, and efficiency. In summary, these findings provide genetic evidence that unveils the indispensable role of maternal Nat10 in oocyte development.
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