Christian earned his PhD in 2011, with the thesis “Roles played by Hfq-like RNA chaperones and sRNAs on the virulence of Burkholderia cepacia complex bacteria”, which was Approved with Honors and Distinction, having published 9 articles in international peer-reviewed journals between 2008 and 2011, focused on molecular mechanisms of virulence. Since 2012, he published 5 articles in international peer-reviewed journals (3 as 1st author - mostly on the molecular mechanisms of the regulatory roles of non-coding RNAs), 3 book chapters, 3 articles in national peer-reviewed journals (2 as 1st author and 1 as co-corresponding author), with a 3-year post-doctoral fellowship by FCT, to pursue a project entitled “Virulence-related sRNAs of B. cenocepacia: Identification, functional analysis and exploitation as novel drug targets”. In the period 2012-14, Christian G. Ramos has been the co-adviser of 2 MSc students, 3 under-graduate students, and has been involved in the mentoring of 2 PhD students. In 2015, CGR took a 3-year position (FCT-funded) in the Gene Expression and Regulation Lab at BioISI, Faculdade de Ciências da Universidade de Lisboa, to embrace a completely new scientific subject. This new project, “Roles of regulatory small ncRNAs in the Modulation of HIV replication and latency”, has allowed the publication of an article in EMBO Journal. CGR has reviewed 12 papers for 5 different journals and has acted as member of the editorial board in 4 journals. In fact, only upon joining the Carmo-Fonseca lab (09/2017) at IMM to work in a European project focused on lysosome biology, in close collaboration with the team of Prof. Futerman (Weizmann Institute, Israel) that CGR started to work on aspects lysosomal biology. Our preliminary data suggest that transcriptional adaptation to heterozygotic mutations play a key role in cellular development, in particular neurogenesis. Therefore, we are using state-of-the-art methods of cellular (live cell fluorescence microscopy) and molecular (RNA-Seq and mNET-Seq) biology to dissect the molecular mechanisms leading to a disease phenotype. My current research interests are focused on the early transcriptional and post-transcriptional adaptation of cells harboring mutations that are known risk factors for Parkinson’s Disease, as is the case of heterozygous GBA. GBA is a lysosomal enzyme responsible for the breakdown of complex lipids. Mounting evidence shows that during aging lysosomes decelerate their critical function in autophagy, that ultimately leads to cellular senescence. It remains to be explained whether dysfunctional lysosomes lead to accelerated aging or is the other way around. In the case of carriers of Gba mutation (heterozygous, since homozygous display Gaucher disease), it has been shown that these otherwise healthy adults develop Parkinson’s disease approximately 10 years before idiopathic patients. Furthermore, in post-mortem brain samples of Parkinson patients, GBA has been found in Lewy bodies, tightly interacting with alpha-synuclein. Although heterozygotic Gba mutation apparently do not lead to any clinical phenotype, reduced lysosomal activity seems to lead to premature neuronal aging, which is arguably more drastic in midbrain dopaminergic neurons. In my hypothesis, since early development, including the oocyte, cells deploy alternative genetic programs to overcome the defects in cellular clearance and autophagy. Therefore, understanding such alternative genetic programs in embryonic stem cells and study their outcome during neurogenesis and neuronal maturation will unveil novel therapeutic target candidates to defray the development of Parkinson’s disease.