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BIOLOGY EXAM II – CLARISSA’S PART 10/16: Pulse Chase, FRAP, Vesicle Transport, SNARES and other proteins involved 10/23: Vesicle Transport, Neurotransmission, sorting, vesicle retrieval system for ER proteins
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BIOLOGY EXAM II – CLARISSA’S PART 10/16: Pulse Chase, FRAP, Vesicle Transport, SNARES and other proteins involved 10/23: Vesicle Transport, Neurotransmission, sorting, vesicle retrieval system for ER proteins 10/27: Pathogen exit and entry (basic differences and how they obtain envelopes); types of retroelements and structures of genomes 10/30: Class I and II transposons; types of retroelements; genome structure and basic replication cycle of a retrovirus; exogenous vs endogenous retroviruses; LINE structure, proteins (function too), and understanding of replication cycle; SINE structure, and understanding of replication cycle 11/06: Evolutionary and genomic consequences of repetitive elements and mobile elements; methylation, proteins involved, and MECP2 function; intrinsic immunity proteins, RNAi and LINES OTHER: The workshop problem set from 11/06 and the Alu problem/question set from 11/03
WHAT ARE THE GENOMIC AND EVOLUTIONARY CONSEQUENCES OF MOBILE ELEMENTS? • Recombination hot spots • Source of transcription promoters • Source of regulatory elements (enhancers and silencers) • Source of protein motifs and new gene functions • Gene silencing
HOW DOES AN ORGANISM CONTROL THESE MOBILE ELEMENTS? • Methylation • Intrinsic immune system • RNAi silencing
Fig. 1, Part 1 METHYLATION PROTECTS AGAINST LINES, SINES, AND ERVs DNA Methylation Reaction Catalyzed by DNA Methyltransferase (DNMT)
Methylation Inhibits LINE Expression And Epigenetic Changes Lead to LINE Expression
INTRINSIC IMMUNE SYSTEM PROTECTS AGAINST ERVs FV4 Cellular Inhibitors of Retrovirus Replication FV1, APOBEC, TRIM5α
TRIM5alpha Binding to Retroviral Capsids Leads to Accelerated Uncoating and Inhibition of RT Emerman. PNAS April 4, 2006 vol. 103 no. 14 5249–5250
APOBEC3G – A Cytidine Deaminase May Inhibit Retroviruses APOBEC3G edits cytosines to uracils in the minus strand DNA copied from the viral RNA genome, resulting in promiscuous guanine-to-adenine (G-to-A) hypermutation of the plus (protein-coding) strand of the viral DNA. Lentiviruses, such as HIV and SIV, encode Vif, a protein that interacts with APOBEC3G and targets it for degradation. Vif of one virus will counteract APOBEC3G from its host species