100+ Free ENADE Ciências Biológicas Practice Questions

Explanation: Cholesterol functions as a bidirectional fluidity buffer in animal cell membranes. At relatively high temperatures (such as 37°C in warm-blooded vertebrates), cholesterol's rigid steroid ring structure hinders excessive lateral movement of phospholipids, thereby decreasing fluidity and permeability. At lower temperatures, cholesterol disrupts the tight regular packing of phospholipid hydrocarbon tails, preventing membrane crystallization/phase transition to a rigid gel state.

Explanation: Secondary active transport via SGLT1 (sodium-glucose linked transporter 1) utilizes the electrochemical potential difference of Na+ across the plasma membrane. This Na+ gradient is continuously established and energized by the primary active transport of the basolateral Na+/K+ ATPase, which pumps 3 Na+ out of the cell and 2 K+ into the cell per hydrolyzed ATP molecule. As Na+ flows down its steep inward electrochemical gradient, glucose is cotransported against its uphill chemical concentration gradient.

Explanation: Targeting of nascent secretory and endomembrane proteins to the rough ER begins when an N-terminal hydrophobic signal peptide emerges from the ribosome exit tunnel. The Signal Recognition Particle (SRP), a ribonucleoprotein complex, binds the signal peptide and temporarily pauses translation elongation. The ribosome-SRP complex then docks with the SRP receptor located on the cytosolic surface of the ER membrane, transferring the nascent chain to the Sec61 aqueous translocon channel for co-translational translocation into the ER lumen.

Explanation: Soluble lysosomal enzymes are tagged in the cis-Golgi apparatus with mannose-6-phosphate (M6P) residues via a two-step enzymatic reaction initiated by GlcNAc-phosphotransferase (UDP-N-acetylglucosamine:lysosomal-enzyme N-acetylglucosaminyl-1-phosphotransferase). Trans-Golgi M6P receptors recognize this modification and sort the hydrolases into clathrin-coated vesicles destined for endosomes/lysosomes. In I-cell disease, deficiency in GlcNAc-phosphotransferase causes lysosomal hydrolases to lack the M6P tag; consequently, they follow the default constitutive secretory pathway and are secreted into the extracellular space, leaving lysosomes empty and full of undegraded inclusion bodies (I-cells).

Explanation: In early G1 phase, the unphosphorylated/hypophosphorylated Retinoblastoma protein (pRb) binds and inhibits the E2F family of transcription factors. In response to mitogenic signaling, Cyclin D levels rise, forming active Cyclin D-CDK4/6 complexes that initiate pRb phosphorylation. Subsequent activation of Cyclin E-CDK2 causes pRb hyperphosphorylation, triggering a conformational change that dissociates pRb from E2F. Free E2F then activates the transcription of essential S-phase genes (including Cyclin E, Cyclin A, and enzymes for dNTP synthesis and DNA replication), driving the cell past the restriction point into S phase.

Explanation: The synaptonemal complex is a tripartite proteinaceous lattice consisting of two lateral elements (derived from axial cores of homologous chromosomes) and a central element linked by transverse filaments. Assembling during the zygotene stage of prophase I, it stabilizes homologous chromosome alignment (synapsis) at an exact ~100 nm spacing, facilitating double-strand break repair and reciprocal homologous recombination (crossing-over) during pachytene.

Explanation: On the eukaryotic lagging strand, DNA polymerase alpha-primase complex synthesizes an initial ~10 nt RNA primer followed by ~20-30 nt of initiator DNA. The sliding clamp PCNA and replicative DNA polymerase delta (Pol delta) take over processive elongation. When Pol delta encounters the 5' end of the downstream Okazaki fragment, it displaces the RNA/DNA primer into a 5' flap. Flap endonuclease 1 (FEN1) (assisted by Dna2 for long flaps) cleaves the flap, and DNA ligase I catalyzes ATP-dependent phosphodiester bond formation to seal the remaining nick.

Explanation: Telomerase is a specialized ribonucleoprotein complex containing a catalytic reverse transcriptase subunit (TERT in humans) and an integral non-coding RNA component (TERC/hTR). TERC provides an internal RNA template complementary to telomeric repeats (5'-TTAGGG-3' in vertebrates). Telomerase binds the 3' protruding single-stranded G-rich overhang of the chromosome and uses its internal RNA template to synthesize tandem telomeric DNA repeats via reverse transcription. Subsequently, standard primase and DNA polymerase alpha/delta synthesize the complementary C-rich strand.

Explanation: RNA Polymerase II (RNA Pol II) is the eukaryotic nuclear enzyme responsible for synthesizing all protein-coding precursor mRNAs, as well as most snRNAs (such as U1, U2, U4, U5 involved in splicing) and microRNAs (miRNAs). In contrast, RNA Polymerase I synthesizes the large ribosomal RNA precursor (28S, 18S, and 5.8S rRNAs), while RNA Polymerase III transcribes transfer RNAs (tRNAs), 5S rRNA, and the U6 snRNA.

Explanation: The spliceosome (composed of U1, U2, U4/U6, and U5 snRNPs) catalyzes pre-mRNA splicing through two sequential transesterification reactions that conserve phosphodiester energy. First, the 2'-hydroxyl group of a specific conserved branch-point adenosine nucleotide makes a nucleophilic attack on the phosphodiester bond at the 5' splice site (GU donor). This cleaves the 5' exon-intron junction and forms a 2'-5' phosphodiester bond, creating a branched 'lariat' intron-exon intermediate. In the second step, the free 3'-hydroxyl of the upstream exon attacks the phosphodiester bond at the 3' splice site (AG acceptor), ligating the two exons together and releasing the excised intron in lariat form.