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花苞缺鐵影響絨氈層功能損害花粉發育

為了解決Sequence Diagram loo的問題，作者黃資翔 這樣論述：

Reduction of crop yield due to iron (Fe) deficiency has always been a concern in agriculture. How insufficient Fe in floral buds affects pollen development remains unexplored. Here, plants transferred to Fe-deficient medium at the reproductive stage had reduced floral Fe content and viable pollen a

nd showed a defective pollen outer wall, all restored by supplying floral buds with Fe. A comparison of differentially expressed genes (DEGs) in Fe-deficient leaves, roots, and anthers suggested that changes in several cellular processes were unique to anthers, including increased lipid degradation.

Co-expression analysis revealed that ABORTED MICROSPORES (AMS), DEFECTIVE IN TAPETAL DEVELOPMENT AND FUNCTION1, and BASIC HELIX-LOOP-HELIX 089/091/010 are key upstream transcription factors of Fe-deficient DEGs involved in tapetum function and development, including tapetal ROS homeostasis, program

med cell death, and pollen outer wall formation-related lipid metabolism. Analysis of RESPIRATORY-BURST OXIDASE HOMOLOG E (RBOHE) gain- and loss-of-function under Fe deficiency indicated that RBOHE- and Fe-dependent regulation coordinated for proper anther ROS and pollen development. Since no DEGs i

n Fe-deficient anthers were significantly enriched in mitochondrial function, the changes in mitochondrial status, including respiration activity, density, and morphology under Fe deficiency were probably because the Fe amount was insufficient to maintain proper mitochondrial protein function in ant

hers. To sum up, Fe deficiency in anthers may affect Fe-dependent protein function and impact upstream transcription factors and their downstream genes to result in extensive impaired tapetum function and pollen development.

鑑定不同癌症中的高突變負擔相關的基因和反應路徑

為了解決Sequence Diagram loo的問題，作者葉大瑋 這樣論述：

在過去的研究中，發現癌症患者的腫瘤突變負荷越高，對癌症免疫療法（尤其是免疫檢查點抑制劑）的反應就越好，使腫瘤突變負荷成為新興的癌症免疫療法的生物標誌。因此，本研究的目標是找到一些與高突變負荷相關的基因。如果可以找到這些與高突變負荷相關的基因，則可以通過檢測這些基因突變的有無，去預估癌症患者是否具有高突變負荷的狀況，並進一步地去推估其是否適合接受免疫療法。這樣能夠降低腫瘤突變負擔在臨床上運用的成本，因為通常腫瘤突變負荷是透過全外顯子定序確定，而這個過程是比較昂貴且耗時的。我們利用了從癌症基因體圖譜計畫取得的體細胞突變的資料，開發了一個方法去找到與高突變負荷相關的基因。首先，利用分段線性回歸的方

式去找到各個癌症樣本的突變負荷數值的轉折點，作為閾值去將樣本分為高突變負荷與低突變負荷。接著，利用費雪正確性檢定去檢驗基因的非同義突變是否與高突變負荷相關。最後再利用基因功能富集分析去找尋與這些高突變負荷相關基因有關的反應路徑。這個方法被應用在25種原發性固態瘤樣本數超過100的癌症，並且在每種癌症中找到一群高突變負荷相關的基因。我們發現有少數基因會在多種癌症中都與高突變負荷顯著相關。然而，這些基因大多數都被發現是長度較長的基因，本身就具有較高的突變率，在這種情況下，這些基因的突變更可能是高突變負荷的結果而非原因。此外，在大多數癌症中這些與高突變負荷相關的基因與細胞發育的功能有關，但目前沒有證

據表示其與突變的增加有關。雖然我們未能找到與高突變負荷形成明顯相關的基因或者是反應路徑，但這些在不同癌症中都與高突變負荷相關的基因還是有希望能成為預測高突變負荷的生物標記，因為他們還是能反映出高突變負荷的結果。若是要尋找導致高突變負荷的基因，在將來可能得用不同的方式進行研究。