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thinker98½ð³æ (ÖøÃûдÊÖ)
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¾ÍÁ½¸öÉó¸åÈË£¬ÆäÖÐÒ»¸öÃ÷ȷдÁËСÐÞ£¬ÁíÒ»¸öÒâ¼ûÈçÏ£¬Òª²¹ÊµÑ飬µ«ÐèÒª²¹µÄʵÑéÎÒÃÇû·¨×ö ......Therefore, the authors carried out a reverse genetic study to clarify the potential function of *** pathway in ***. They first came out a working model and then tested it step by step. The results were all perfectly supportive to their model and they concluded that***. The study is of interests and may have implication in understanding the molecular mechanism underlying ***. However, my concern is that their experiments only focused on the working model, which may cause some biases in the result interpretation. For example, if they did not compare the activities of other signaling pathways (including but not limited to MAKP and Insulin pathways) in the ***, how do they know whether lower *** pathway activity in the *** is the major REASON of *** or it is the RESULT of d*** common to most signaling pathways? I will suggest two experiments. 1). Functional test for *** in pupal development (such as RNAi knock-down of <beta>-catenin and myc in non-diapause pupae). 2). Comparative study of other signaling pathway activities in the *** (such as RNA-seq). |
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3Â¥2014-05-28 18:14:45
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2Â¥2014-05-28 17:58:28
fengspring
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4Â¥2014-05-28 18:20:42
thinker98
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